---
_id: '60182'
author:
- first_name: I
full_name: Perrar, I
last_name: Perrar
- first_name: E
full_name: Hohoff, E
last_name: Hohoff
- first_name: A
full_name: Lesani, A
last_name: Lesani
- first_name: S
full_name: Schmitting, S
last_name: Schmitting
- first_name: Lars
full_name: Libuda, Lars
id: '88682'
last_name: Libuda
orcid: 0000-0003-1603-3133
- first_name: Bettina
full_name: Krüger, Bettina
id: '49428'
last_name: Krüger
orcid: 0000-0001-5351-1785
- first_name: Bianca
full_name: Stutz, Bianca
id: '77099'
last_name: Stutz
- first_name: U
full_name: Nöthlings, U
last_name: Nöthlings
- first_name: Anette
full_name: Buyken, Anette
id: '65985'
last_name: Buyken
- first_name: U
full_name: Alexy, U
last_name: Alexy
- first_name: N
full_name: Jankovic, N
last_name: Jankovic
citation:
ama: Perrar I, Hohoff E, Lesani A, et al. Circadian eating patterns track from infancy
to pre- and primary school-age, but are not prospectively associated with body
composition in childhood - Results of the DONALD cohort study. Eur J Nutr.
2025;64(4):165.
apa: Perrar, I., Hohoff, E., Lesani, A., Schmitting, S., Libuda, L., Krüger, B.,
Stutz, B., Nöthlings, U., Buyken, A., Alexy, U., & Jankovic, N. (2025). Circadian
eating patterns track from infancy to pre- and primary school-age, but are not
prospectively associated with body composition in childhood - Results of the DONALD
cohort study. Eur J Nutr, 64(4), 165.
bibtex: '@article{Perrar_Hohoff_Lesani_Schmitting_Libuda_Krüger_Stutz_Nöthlings_Buyken_Alexy_et
al._2025, title={Circadian eating patterns track from infancy to pre- and primary
school-age, but are not prospectively associated with body composition in childhood
- Results of the DONALD cohort study.}, volume={64}, number={4}, journal={Eur
J Nutr}, author={Perrar, I and Hohoff, E and Lesani, A and Schmitting, S and Libuda,
Lars and Krüger, Bettina and Stutz, Bianca and Nöthlings, U and Buyken, Anette
and Alexy, U and et al.}, year={2025}, pages={165} }'
chicago: 'Perrar, I, E Hohoff, A Lesani, S Schmitting, Lars Libuda, Bettina Krüger,
Bianca Stutz, et al. “Circadian Eating Patterns Track from Infancy to Pre- and
Primary School-Age, but Are Not Prospectively Associated with Body Composition
in Childhood - Results of the DONALD Cohort Study.” Eur J Nutr 64, no.
4 (2025): 165.'
ieee: I. Perrar et al., “Circadian eating patterns track from infancy to
pre- and primary school-age, but are not prospectively associated with body composition
in childhood - Results of the DONALD cohort study.,” Eur J Nutr, vol. 64,
no. 4, p. 165, 2025.
mla: Perrar, I., et al. “Circadian Eating Patterns Track from Infancy to Pre- and
Primary School-Age, but Are Not Prospectively Associated with Body Composition
in Childhood - Results of the DONALD Cohort Study.” Eur J Nutr, vol. 64,
no. 4, 2025, p. 165.
short: I. Perrar, E. Hohoff, A. Lesani, S. Schmitting, L. Libuda, B. Krüger, B.
Stutz, U. Nöthlings, A. Buyken, U. Alexy, N. Jankovic, Eur J Nutr 64 (2025) 165.
date_created: 2025-06-11T08:49:19Z
date_updated: 2025-06-11T08:51:28Z
department:
- _id: '22'
external_id:
pmid:
- '40285866'
intvolume: ' 64'
issue: '4'
language:
- iso: eng
page: '165'
pmid: '1'
publication: Eur J Nutr
publication_identifier:
issn:
- 1436-6207
- 1436-6215
status: public
title: Circadian eating patterns track from infancy to pre- and primary school-age,
but are not prospectively associated with body composition in childhood - Results
of the DONALD cohort study.
type: journal_article
user_id: '92491'
volume: 64
year: '2025'
...
---
_id: '60873'
abstract:
- lang: eng
text: "Abstract\r\n Variations in circadian
rhythm-related genes influence the individual chronotype. Here, we hypothesize
that the peak of clock gene expression at 7 a.m. differs between young adults
with a late chronotype and young adults with an early chronotype. Participants
of the Chronotype and Nutrition nutritional trial (ChroNu study) were selected
for their chronotype assessed by the Munich Chronotype questionnaire (MCTQ) and
actigraphy. Total RNA was isolated from CD14+ monocytes of
participants at 7 a.m. on the run-in day. Expression levels of seven clock genes
(PER1, PER2,
PER3, NR1D1, NR1D2,
CRY1 and CRISPLD2) of individuals
with early (n = 11) or late chronotypes (n = 19)
were analysed by reverse transcription quantitative polymerase chain reaction.
Difference in expression levels was tested by Mann Whitney-U test. The relative
expression levels of the selected genes were not significantly different between
individuals with early and late chronotypes (all p > 0.07).
Contrary to expectation, clock gene expression levels at 7 a.m. was similar in
individuals with early and late chronotypes. Further studies on larger sample
sizes with multiple sampling time points should elucidate whether gene expression
is altered at other day times underscoring the biological difference between individuals
with early or late chronotypes."
article_number: '26709'
author:
- first_name: Bettina
full_name: Krueger, Bettina
id: '49428'
last_name: Krueger
orcid: 0000-0001-5351-1785
- first_name: Luisa Sophie
full_name: Rajcsanyi, Luisa Sophie
last_name: Rajcsanyi
- first_name: Katharina
full_name: Hundertmark, Katharina
last_name: Hundertmark
- first_name: Bianca
full_name: Stutz, Bianca
id: '77099'
last_name: Stutz
- first_name: Anke
full_name: Hinney, Anke
last_name: Hinney
- first_name: Anette E.
full_name: Buyken, Anette E.
id: '65985'
last_name: Buyken
citation:
ama: Krueger B, Rajcsanyi LS, Hundertmark K, Stutz B, Hinney A, Buyken AE. Morning
clock gene expression in young adults of early and late chronotypes. Scientific
Reports. 2025;15(1). doi:10.1038/s41598-025-12423-7
apa: Krueger, B., Rajcsanyi, L. S., Hundertmark, K., Stutz, B., Hinney, A., &
Buyken, A. E. (2025). Morning clock gene expression in young adults of early and
late chronotypes. Scientific Reports, 15(1), Article 26709. https://doi.org/10.1038/s41598-025-12423-7
bibtex: '@article{Krueger_Rajcsanyi_Hundertmark_Stutz_Hinney_Buyken_2025, title={Morning
clock gene expression in young adults of early and late chronotypes}, volume={15},
DOI={10.1038/s41598-025-12423-7},
number={126709}, journal={Scientific Reports}, publisher={Springer Science and
Business Media LLC}, author={Krueger, Bettina and Rajcsanyi, Luisa Sophie and
Hundertmark, Katharina and Stutz, Bianca and Hinney, Anke and Buyken, Anette E.},
year={2025} }'
chicago: Krueger, Bettina, Luisa Sophie Rajcsanyi, Katharina Hundertmark, Bianca
Stutz, Anke Hinney, and Anette E. Buyken. “Morning Clock Gene Expression in Young
Adults of Early and Late Chronotypes.” Scientific Reports 15, no. 1 (2025).
https://doi.org/10.1038/s41598-025-12423-7.
ieee: 'B. Krueger, L. S. Rajcsanyi, K. Hundertmark, B. Stutz, A. Hinney, and A.
E. Buyken, “Morning clock gene expression in young adults of early and late chronotypes,”
Scientific Reports, vol. 15, no. 1, Art. no. 26709, 2025, doi: 10.1038/s41598-025-12423-7.'
mla: Krueger, Bettina, et al. “Morning Clock Gene Expression in Young Adults of
Early and Late Chronotypes.” Scientific Reports, vol. 15, no. 1, 26709,
Springer Science and Business Media LLC, 2025, doi:10.1038/s41598-025-12423-7.
short: B. Krueger, L.S. Rajcsanyi, K. Hundertmark, B. Stutz, A. Hinney, A.E. Buyken,
Scientific Reports 15 (2025).
date_created: 2025-08-05T05:17:48Z
date_updated: 2025-08-05T05:19:20Z
department:
- _id: '35'
- _id: '22'
doi: 10.1038/s41598-025-12423-7
intvolume: ' 15'
issue: '1'
language:
- iso: eng
publication: Scientific Reports
publication_identifier:
issn:
- 2045-2322
publication_status: published
publisher: Springer Science and Business Media LLC
status: public
title: Morning clock gene expression in young adults of early and late chronotypes
type: journal_article
user_id: '49428'
volume: 15
year: '2025'
...
---
_id: '54926'
author:
- first_name: Bianca
full_name: Stutz, Bianca
id: '77099'
last_name: Stutz
- first_name: Bettina
full_name: Krueger, Bettina
id: '49428'
last_name: Krueger
orcid: 0000-0001-5351-1785
- first_name: Janina
full_name: Goletzke, Janina
last_name: Goletzke
- first_name: Nicole
full_name: Jankovic, Nicole
last_name: Jankovic
- first_name: Ute
full_name: Alexy, Ute
last_name: Alexy
- first_name: Christian
full_name: Herder, Christian
last_name: Herder
- first_name: Jutta
full_name: Dierkes, Jutta
last_name: Dierkes
- first_name: Gabriele
full_name: Berg-Beckhoff, Gabriele
last_name: Berg-Beckhoff
- first_name: Rasmus
full_name: Jakobsmeyer, Rasmus
id: '9583'
last_name: Jakobsmeyer
orcid: 0000-0002-9385-0834
- first_name: Claus
full_name: Reinsberger, Claus
id: '48978'
last_name: Reinsberger
- first_name: Anette E.
full_name: Buyken, Anette E.
id: '65985'
last_name: Buyken
citation:
ama: 'Stutz B, Krueger B, Goletzke J, et al. Glycemic response to meals with a high
glycemic index differs between morning and evening: a randomized cross-over controlled
trial among students with early or late chronotype. European Journal of Nutrition.
Published online 2024. doi:10.1007/s00394-024-03372-4'
apa: 'Stutz, B., Krueger, B., Goletzke, J., Jankovic, N., Alexy, U., Herder, C.,
Dierkes, J., Berg-Beckhoff, G., Jakobsmeyer, R., Reinsberger, C., & Buyken,
A. E. (2024). Glycemic response to meals with a high glycemic index differs between
morning and evening: a randomized cross-over controlled trial among students with
early or late chronotype. European Journal of Nutrition. https://doi.org/10.1007/s00394-024-03372-4'
bibtex: '@article{Stutz_Krueger_Goletzke_Jankovic_Alexy_Herder_Dierkes_Berg-Beckhoff_Jakobsmeyer_Reinsberger_et
al._2024, title={Glycemic response to meals with a high glycemic index differs
between morning and evening: a randomized cross-over controlled trial among students
with early or late chronotype}, DOI={10.1007/s00394-024-03372-4},
journal={European Journal of Nutrition}, publisher={Springer}, author={Stutz,
Bianca and Krueger, Bettina and Goletzke, Janina and Jankovic, Nicole and Alexy,
Ute and Herder, Christian and Dierkes, Jutta and Berg-Beckhoff, Gabriele and Jakobsmeyer,
Rasmus and Reinsberger, Claus and et al.}, year={2024} }'
chicago: 'Stutz, Bianca, Bettina Krueger, Janina Goletzke, Nicole Jankovic, Ute
Alexy, Christian Herder, Jutta Dierkes, et al. “Glycemic Response to Meals with
a High Glycemic Index Differs between Morning and Evening: A Randomized Cross-over
Controlled Trial among Students with Early or Late Chronotype.” European Journal
of Nutrition, 2024. https://doi.org/10.1007/s00394-024-03372-4.'
ieee: 'B. Stutz et al., “Glycemic response to meals with a high glycemic
index differs between morning and evening: a randomized cross-over controlled
trial among students with early or late chronotype,” European Journal of Nutrition,
2024, doi: 10.1007/s00394-024-03372-4.'
mla: 'Stutz, Bianca, et al. “Glycemic Response to Meals with a High Glycemic Index
Differs between Morning and Evening: A Randomized Cross-over Controlled Trial
among Students with Early or Late Chronotype.” European Journal of Nutrition,
Springer, 2024, doi:10.1007/s00394-024-03372-4.'
short: B. Stutz, B. Krueger, J. Goletzke, N. Jankovic, U. Alexy, C. Herder, J. Dierkes,
G. Berg-Beckhoff, R. Jakobsmeyer, C. Reinsberger, A.E. Buyken, European Journal
of Nutrition (2024).
date_created: 2024-06-30T13:38:17Z
date_updated: 2024-06-30T13:39:12Z
department:
- _id: '35'
- _id: '22'
doi: 10.1007/s00394-024-03372-4
language:
- iso: eng
publication: European Journal of Nutrition
publication_identifier:
issn:
- 1436-6215
publisher: Springer
status: public
title: 'Glycemic response to meals with a high glycemic index differs between morning
and evening: a randomized cross-over controlled trial among students with early
or late chronotype'
type: journal_article
user_id: '49428'
year: '2024'
...
---
_id: '54927'
author:
- first_name: Bianca
full_name: Stutz, Bianca
id: '77099'
last_name: Stutz
- first_name: Janina
full_name: Goletzke, Janina
last_name: Goletzke
- first_name: Bettina
full_name: Krueger, Bettina
id: '49428'
last_name: Krueger
orcid: 0000-0001-5351-1785
- first_name: Nicole
full_name: Jankovic, Nicole
id: '105192'
last_name: Jankovic
orcid: https://orcid.org/0000-0002-9235-5356
- first_name: Ute
full_name: Alexy, Ute
last_name: Alexy
- first_name: Christian
full_name: Herder, Christian
last_name: Herder
- first_name: Rasmus
full_name: Jakobsmeyer, Rasmus
id: '9583'
last_name: Jakobsmeyer
orcid: 0000-0002-9385-0834
- first_name: Claus
full_name: Reinsberger, Claus
id: '48978'
last_name: Reinsberger
- first_name: Anette E.
full_name: Buyken, Anette E.
id: '65985'
last_name: Buyken
citation:
ama: Stutz B, Goletzke J, Krueger B, et al. Association between glucose dips and
the feeling of hunger in a dietary intervention study among students with early
and late chronotype-secondary analysis of a randomized cross-over nutrition trial.
Appetite. 2024;200:107569. doi:10.1016/j.appet.2024.107569
apa: Stutz, B., Goletzke, J., Krueger, B., Jankovic, N., Alexy, U., Herder, C.,
Jakobsmeyer, R., Reinsberger, C., & Buyken, A. E. (2024). Association between
glucose dips and the feeling of hunger in a dietary intervention study among students
with early and late chronotype-secondary analysis of a randomized cross-over nutrition
trial. Appetite, 200, 107569. https://doi.org/10.1016/j.appet.2024.107569
bibtex: '@article{Stutz_Goletzke_Krueger_Jankovic_Alexy_Herder_Jakobsmeyer_Reinsberger_Buyken_2024,
title={Association between glucose dips and the feeling of hunger in a dietary
intervention study among students with early and late chronotype-secondary analysis
of a randomized cross-over nutrition trial}, volume={200}, DOI={10.1016/j.appet.2024.107569},
journal={Appetite}, publisher={Elsevier}, author={Stutz, Bianca and Goletzke,
Janina and Krueger, Bettina and Jankovic, Nicole and Alexy, Ute and Herder, Christian
and Jakobsmeyer, Rasmus and Reinsberger, Claus and Buyken, Anette E.}, year={2024},
pages={107569} }'
chicago: 'Stutz, Bianca, Janina Goletzke, Bettina Krueger, Nicole Jankovic, Ute
Alexy, Christian Herder, Rasmus Jakobsmeyer, Claus Reinsberger, and Anette E.
Buyken. “Association between Glucose Dips and the Feeling of Hunger in a Dietary
Intervention Study among Students with Early and Late Chronotype-Secondary Analysis
of a Randomized Cross-over Nutrition Trial.” Appetite 200 (2024): 107569.
https://doi.org/10.1016/j.appet.2024.107569.'
ieee: 'B. Stutz et al., “Association between glucose dips and the feeling
of hunger in a dietary intervention study among students with early and late chronotype-secondary
analysis of a randomized cross-over nutrition trial,” Appetite, vol. 200,
p. 107569, 2024, doi: 10.1016/j.appet.2024.107569.'
mla: Stutz, Bianca, et al. “Association between Glucose Dips and the Feeling of
Hunger in a Dietary Intervention Study among Students with Early and Late Chronotype-Secondary
Analysis of a Randomized Cross-over Nutrition Trial.” Appetite, vol. 200,
Elsevier, 2024, p. 107569, doi:10.1016/j.appet.2024.107569.
short: B. Stutz, J. Goletzke, B. Krueger, N. Jankovic, U. Alexy, C. Herder, R. Jakobsmeyer,
C. Reinsberger, A.E. Buyken, Appetite 200 (2024) 107569.
date_created: 2024-06-30T13:40:19Z
date_updated: 2024-06-30T13:41:10Z
department:
- _id: '35'
- _id: '22'
doi: 10.1016/j.appet.2024.107569
intvolume: ' 200'
language:
- iso: eng
page: '107569'
publication: Appetite
publisher: Elsevier
status: public
title: Association between glucose dips and the feeling of hunger in a dietary intervention
study among students with early and late chronotype-secondary analysis of a randomized
cross-over nutrition trial
type: journal_article
user_id: '49428'
volume: 200
year: '2024'
...
---
_id: '57429'
author:
- first_name: Bettina
full_name: Krueger, Bettina
id: '49428'
last_name: Krueger
orcid: 0000-0001-5351-1785
- first_name: Bianca
full_name: Stutz, Bianca
id: '77099'
last_name: Stutz
- first_name: Rasmus
full_name: Jakobsmeyer, Rasmus
id: '9583'
last_name: Jakobsmeyer
orcid: 0000-0002-9385-0834
- first_name: Claus
full_name: Reinsberger, Claus
id: '48978'
last_name: Reinsberger
- first_name: Anette E.
full_name: Buyken, Anette E.
id: '65985'
last_name: Buyken
citation:
ama: Krueger B, Stutz B, Jakobsmeyer R, Reinsberger C, Buyken AE. Relevance of high
glycaemic index breakfast for heart rate variability among collegiate students
with early and late chronotypes. Chronobiology International. Published
online 2024:1-10. doi:10.1080/07420528.2024.2428203
apa: Krueger, B., Stutz, B., Jakobsmeyer, R., Reinsberger, C., & Buyken, A.
E. (2024). Relevance of high glycaemic index breakfast for heart rate variability
among collegiate students with early and late chronotypes. Chronobiology International,
1–10. https://doi.org/10.1080/07420528.2024.2428203
bibtex: '@article{Krueger_Stutz_Jakobsmeyer_Reinsberger_Buyken_2024, title={Relevance
of high glycaemic index breakfast for heart rate variability among collegiate
students with early and late chronotypes}, DOI={10.1080/07420528.2024.2428203},
journal={Chronobiology International}, publisher={Informa UK Limited}, author={Krueger,
Bettina and Stutz, Bianca and Jakobsmeyer, Rasmus and Reinsberger, Claus and Buyken,
Anette E.}, year={2024}, pages={1–10} }'
chicago: Krueger, Bettina, Bianca Stutz, Rasmus Jakobsmeyer, Claus Reinsberger,
and Anette E. Buyken. “Relevance of High Glycaemic Index Breakfast for Heart Rate
Variability among Collegiate Students with Early and Late Chronotypes.” Chronobiology
International, 2024, 1–10. https://doi.org/10.1080/07420528.2024.2428203.
ieee: 'B. Krueger, B. Stutz, R. Jakobsmeyer, C. Reinsberger, and A. E. Buyken, “Relevance
of high glycaemic index breakfast for heart rate variability among collegiate
students with early and late chronotypes,” Chronobiology International,
pp. 1–10, 2024, doi: 10.1080/07420528.2024.2428203.'
mla: Krueger, Bettina, et al. “Relevance of High Glycaemic Index Breakfast for Heart
Rate Variability among Collegiate Students with Early and Late Chronotypes.” Chronobiology
International, Informa UK Limited, 2024, pp. 1–10, doi:10.1080/07420528.2024.2428203.
short: B. Krueger, B. Stutz, R. Jakobsmeyer, C. Reinsberger, A.E. Buyken, Chronobiology
International (2024) 1–10.
date_created: 2024-11-26T10:51:33Z
date_updated: 2024-11-26T10:52:50Z
department:
- _id: '35'
- _id: '22'
doi: 10.1080/07420528.2024.2428203
language:
- iso: eng
page: 1-10
publication: Chronobiology International
publication_identifier:
issn:
- 0742-0528
- 1525-6073
publication_status: published
publisher: Informa UK Limited
status: public
title: Relevance of high glycaemic index breakfast for heart rate variability among
collegiate students with early and late chronotypes
type: journal_article
user_id: '49428'
year: '2024'
...
---
_id: '36073'
author:
- first_name: Bianca
full_name: Stutz, Bianca
last_name: Stutz
- first_name: Anette E.
full_name: Buyken, Anette E.
id: '65985'
last_name: Buyken
- first_name: Alena
full_name: Schadow, Alena
last_name: Schadow
- first_name: N
full_name: Jankovic, N
last_name: Jankovic
- first_name: U
full_name: Alexy, U
last_name: Alexy
- first_name: Betina
full_name: Krueger, Betina
id: '49428'
last_name: Krueger
orcid: 0000-0001-5351-1785
citation:
ama: Stutz B, Buyken AE, Schadow A, Jankovic N, Alexy U, Krueger B. Associations
of chronotype and social jetlag with eating jetlag and their changes among German
students during the first COVID-19 lockdown. The Chronotype and Nutrition study.
Appetite. 2023;180:106333. doi:10.1016/j.appet.2022.106333
apa: Stutz, B., Buyken, A. E., Schadow, A., Jankovic, N., Alexy, U., & Krueger,
B. (2023). Associations of chronotype and social jetlag with eating jetlag and
their changes among German students during the first COVID-19 lockdown. The Chronotype
and Nutrition study. Appetite, 180, 106333. https://doi.org/10.1016/j.appet.2022.106333
bibtex: '@article{Stutz_Buyken_Schadow_Jankovic_Alexy_Krueger_2023, title={Associations
of chronotype and social jetlag with eating jetlag and their changes among German
students during the first COVID-19 lockdown. The Chronotype and Nutrition study.},
volume={180}, DOI={10.1016/j.appet.2022.106333},
journal={Appetite}, author={Stutz, Bianca and Buyken, Anette E. and Schadow, Alena
and Jankovic, N and Alexy, U and Krueger, Betina}, year={2023}, pages={106333}
}'
chicago: 'Stutz, Bianca, Anette E. Buyken, Alena Schadow, N Jankovic, U Alexy, and
Betina Krueger. “Associations of Chronotype and Social Jetlag with Eating Jetlag
and Their Changes among German Students during the First COVID-19 Lockdown. The
Chronotype and Nutrition Study.” Appetite 180 (2023): 106333. https://doi.org/10.1016/j.appet.2022.106333.'
ieee: 'B. Stutz, A. E. Buyken, A. Schadow, N. Jankovic, U. Alexy, and B. Krueger,
“Associations of chronotype and social jetlag with eating jetlag and their changes
among German students during the first COVID-19 lockdown. The Chronotype and Nutrition
study.,” Appetite, vol. 180, p. 106333, 2023, doi: 10.1016/j.appet.2022.106333.'
mla: Stutz, Bianca, et al. “Associations of Chronotype and Social Jetlag with Eating
Jetlag and Their Changes among German Students during the First COVID-19 Lockdown.
The Chronotype and Nutrition Study.” Appetite, vol. 180, 2023, p. 106333,
doi:10.1016/j.appet.2022.106333.
short: B. Stutz, A.E. Buyken, A. Schadow, N. Jankovic, U. Alexy, B. Krueger, Appetite
180 (2023) 106333.
date_created: 2023-01-11T11:49:31Z
date_updated: 2023-01-13T07:17:08Z
department:
- _id: '17'
doi: 10.1016/j.appet.2022.106333
external_id:
pmid:
- '36202148'
intvolume: ' 180'
language:
- iso: eng
page: '106333'
pmid: '1'
publication: Appetite
publication_identifier:
issn:
- 0195-6663
- 1095-8304
status: public
title: Associations of chronotype and social jetlag with eating jetlag and their changes
among German students during the first COVID-19 lockdown. The Chronotype and Nutrition
study.
type: journal_article
user_id: '49428'
volume: 180
year: '2023'
...
---
_id: '48456'
abstract:
- lang: eng
text: "Abstract\r\n Purpose\r\n
\ Our aim was to assess alignment in timing of ‘highest caloric
intake’ with individual chronotype and its association with body composition in
adolescents.\r\n \r\n Methods\r\n
\ We used repeatedly collected data from n = 196
adolescents (age 9–16 years, providing N = 401 yearly
questionnaires) of the DONALD open cohort study. Chronotype was assessed by the
Munich Chronotype Questionnaire from which midpoint of sleep (MSFsc) was derived.
A sex- and age-specific diet-chrono-alignment score (DCAS) was calculated as the
difference in hours between the chronotype-specific median timing of highest caloric
intake of the studied population and the individual timing of ‘highest caloric
intake’ or vice versa. Repeated-measures regression models were applied to study
cross-sectional and longitudinal associations between the DCAS and body composition,
e.g., Fat Mass Index (FMI) or Fat Free Mass Index (FFMI).\r\n \r\n
\ Results\r\n DCAS ranged
from −6:42 h to + 8:01 h and was not associated with body composition. Among adolescents
with a later chronotype (N = 201) a 1 h increase in
DCAS (later consumption of ‘highest caloric intake’ in comparison to the median
intake of that group), increased FFMI by 1.92 kg/m2 (95%
CI: 0.15, 3.69, p value = 0.04) over a median follow-up
of 0.94 year.\r\n \r\n Conclusion\r\n
\ Alignment of energy intake with individual chronotype appears
beneficial for FFMI among those with a late chronotype.\r\n "
author:
- first_name: Nicole
full_name: Jankovic, Nicole
last_name: Jankovic
- first_name: Sarah
full_name: Schmitting, Sarah
last_name: Schmitting
- first_name: Bianca
full_name: Stutz, Bianca
id: '77099'
last_name: Stutz
- first_name: Bettina
full_name: Krüger, Bettina
id: '49428'
last_name: Krüger
orcid: 0000-0001-5351-1785
- first_name: Anette
full_name: Buyken, Anette
id: '65985'
last_name: Buyken
- first_name: Ute
full_name: Alexy, Ute
last_name: Alexy
citation:
ama: 'Jankovic N, Schmitting S, Stutz B, Krüger B, Buyken A, Alexy U. Alignment
between timing of ‘highest caloric intake’ and chronotype in relation to body
composition during adolescence: the DONALD Study. European Journal of Nutrition.
Published online 2023. doi:10.1007/s00394-023-03259-w'
apa: 'Jankovic, N., Schmitting, S., Stutz, B., Krüger, B., Buyken, A., & Alexy,
U. (2023). Alignment between timing of ‘highest caloric intake’ and chronotype
in relation to body composition during adolescence: the DONALD Study. European
Journal of Nutrition. https://doi.org/10.1007/s00394-023-03259-w'
bibtex: '@article{Jankovic_Schmitting_Stutz_Krüger_Buyken_Alexy_2023, title={Alignment
between timing of ‘highest caloric intake’ and chronotype in relation to body
composition during adolescence: the DONALD Study}, DOI={10.1007/s00394-023-03259-w},
journal={European Journal of Nutrition}, publisher={Springer Science and Business
Media LLC}, author={Jankovic, Nicole and Schmitting, Sarah and Stutz, Bianca and
Krüger, Bettina and Buyken, Anette and Alexy, Ute}, year={2023} }'
chicago: 'Jankovic, Nicole, Sarah Schmitting, Bianca Stutz, Bettina Krüger, Anette
Buyken, and Ute Alexy. “Alignment between Timing of ‘Highest Caloric Intake’ and
Chronotype in Relation to Body Composition during Adolescence: The DONALD Study.”
European Journal of Nutrition, 2023. https://doi.org/10.1007/s00394-023-03259-w.'
ieee: 'N. Jankovic, S. Schmitting, B. Stutz, B. Krüger, A. Buyken, and U. Alexy,
“Alignment between timing of ‘highest caloric intake’ and chronotype in relation
to body composition during adolescence: the DONALD Study,” European Journal
of Nutrition, 2023, doi: 10.1007/s00394-023-03259-w.'
mla: 'Jankovic, Nicole, et al. “Alignment between Timing of ‘Highest Caloric Intake’
and Chronotype in Relation to Body Composition during Adolescence: The DONALD
Study.” European Journal of Nutrition, Springer Science and Business Media
LLC, 2023, doi:10.1007/s00394-023-03259-w.'
short: N. Jankovic, S. Schmitting, B. Stutz, B. Krüger, A. Buyken, U. Alexy, European
Journal of Nutrition (2023).
date_created: 2023-10-25T08:38:46Z
date_updated: 2023-10-25T08:39:21Z
department:
- _id: '22'
doi: 10.1007/s00394-023-03259-w
keyword:
- Nutrition and Dietetics
- Medicine (miscellaneous)
language:
- iso: eng
publication: European Journal of Nutrition
publication_identifier:
issn:
- 1436-6207
- 1436-6215
publication_status: published
publisher: Springer Science and Business Media LLC
status: public
title: 'Alignment between timing of ‘highest caloric intake’ and chronotype in relation
to body composition during adolescence: the DONALD Study'
type: journal_article
user_id: '92491'
year: '2023'
...
---
_id: '36505'
abstract:
- lang: eng
text: Young adults with a later chronotype are vulnerable for a discrepancy
in sleep rhythm between work- and free days, called social jet lag (SJL). This
study analysed (i) chronotype/SJL association with visceral fat/skeletal muscle
mass, (ii) the attribution to physical activity behaviour, and (iii) chronotype-specific
changes in physical activity behaviour in young adults during the Covid-19 pandemic
lockdown. Chronotype and SJL were derived from the Munich-Chrono-Type-Questionnaire
in 320 German students (age 18–25 years) from September 2019 to January 2020,
156 of these participated in an online follow-up survey in June 2020. Body composition
was assessed by bioimpedance analysis at baseline. Multivariable linear regression
analyses were used to relate chronotype/SJL to body composition; the contribution
of self-reported physical activity was tested by mediation analysis. At baseline,
a later chronotype and a larger SJL were associated with a higher visceral fat
mass (P<0.05), this relation was notably mediated by the attention to physical
activity (P<0.05). Chronotype (P = 0.02) but not SJL (P = 0.87) was inversely
associated with skeletal muscle mass. During the pandemic lockdown, chronotype
hardly changed, but SJL was reduced. Timing and physical activity behaviour remained
in most participants and changes were unrelated to chronotype (all P>0.07).
A later chronotype/higher SJL may increase the risk of a higher visceral fat mass
even in this relatively healthy sample, which may be partly due to their physical
activity behaviour. Despite a reduction in SJL during the pandemic lockdown, later
chronotypes did not change their physical activity behaviour more than earlier
chronotypes.
article_number: e0279620
author:
- first_name: Betina
full_name: Krueger, Betina
id: '49428'
last_name: Krueger
orcid: 0000-0001-5351-1785
- first_name: Bianca
full_name: Stutz, Bianca
id: '77099'
last_name: Stutz
- first_name: Nicole
full_name: Jankovic, Nicole
last_name: Jankovic
- first_name: Ute
full_name: Alexy, Ute
last_name: Alexy
- first_name: Anna
full_name: Kilanowski, Anna
last_name: Kilanowski
- first_name: Lars
full_name: Libuda, Lars
id: '88682'
last_name: Libuda
orcid: 0000-0003-1603-3133
- first_name: Anette E.
full_name: Buyken, Anette E.
id: '65985'
last_name: Buyken
citation:
ama: 'Krueger B, Stutz B, Jankovic N, et al. The association of chronotype and social
jet lag with body composition in German students: The role of physical activity
behaviour and the impact of the pandemic lockdown. PLOS ONE. 2023;18(1).
doi:10.1371/journal.pone.0279620'
apa: 'Krueger, B., Stutz, B., Jankovic, N., Alexy, U., Kilanowski, A., Libuda, L.,
& Buyken, A. E. (2023). The association of chronotype and social jet lag with
body composition in German students: The role of physical activity behaviour and
the impact of the pandemic lockdown. PLOS ONE, 18(1), Article e0279620.
https://doi.org/10.1371/journal.pone.0279620'
bibtex: '@article{Krueger_Stutz_Jankovic_Alexy_Kilanowski_Libuda_Buyken_2023, title={The
association of chronotype and social jet lag with body composition in German students:
The role of physical activity behaviour and the impact of the pandemic lockdown},
volume={18}, DOI={10.1371/journal.pone.0279620},
number={1e0279620}, journal={PLOS ONE}, publisher={Public Library of Science (PLoS)},
author={Krueger, Betina and Stutz, Bianca and Jankovic, Nicole and Alexy, Ute
and Kilanowski, Anna and Libuda, Lars and Buyken, Anette E.}, year={2023} }'
chicago: 'Krueger, Betina, Bianca Stutz, Nicole Jankovic, Ute Alexy, Anna Kilanowski,
Lars Libuda, and Anette E. Buyken. “The Association of Chronotype and Social Jet
Lag with Body Composition in German Students: The Role of Physical Activity Behaviour
and the Impact of the Pandemic Lockdown.” PLOS ONE 18, no. 1 (2023). https://doi.org/10.1371/journal.pone.0279620.'
ieee: 'B. Krueger et al., “The association of chronotype and social jet lag
with body composition in German students: The role of physical activity behaviour
and the impact of the pandemic lockdown,” PLOS ONE, vol. 18, no. 1, Art.
no. e0279620, 2023, doi: 10.1371/journal.pone.0279620.'
mla: 'Krueger, Betina, et al. “The Association of Chronotype and Social Jet Lag
with Body Composition in German Students: The Role of Physical Activity Behaviour
and the Impact of the Pandemic Lockdown.” PLOS ONE, vol. 18, no. 1, e0279620,
Public Library of Science (PLoS), 2023, doi:10.1371/journal.pone.0279620.'
short: B. Krueger, B. Stutz, N. Jankovic, U. Alexy, A. Kilanowski, L. Libuda, A.E.
Buyken, PLOS ONE 18 (2023).
date_created: 2023-01-13T07:15:13Z
date_updated: 2023-01-24T11:54:46Z
department:
- _id: '35'
- _id: '22'
doi: 10.1371/journal.pone.0279620
intvolume: ' 18'
issue: '1'
keyword:
- Multidisciplinary
language:
- iso: eng
publication: PLOS ONE
publication_identifier:
issn:
- 1932-6203
publication_status: published
publisher: Public Library of Science (PLoS)
status: public
title: 'The association of chronotype and social jet lag with body composition in
German students: The role of physical activity behaviour and the impact of the pandemic
lockdown'
type: journal_article
user_id: '61597'
volume: 18
year: '2023'
...
---
_id: '27114'
abstract:
- lang: eng
text: "Abstract\r\n Background/objectives\r\n
\ Adolescence is a critical period for both the development
of overweight and the transition toward a later chronotype, often accompanied
by an increase in social jetlag. This study assessed whether changes in chronotype
and social jetlag, are linked to changes in body composition during adolescence.\r\n
\ \r\n Subjects/methods\r\n
\ We used data from the DONALD open cohort study, collected
between 2014 and 2019, from 213 adolescents (9–17 years at baseline, 45% females)
having at least two measures of chronotype and anthropometry (N = 572).
Chronotype was assessed with the Munich Chronotype Questionnaire and defined as:
midpoint of sleep corrected for sleep-debt (MSFsc) accumulated over the week (later
MSFsc represents later chronotype). Social jetlag (SJL) defines the difference
between midpoint of sleep during week and weekend. Calculations for Fat Free Mass
Index (FFMI [kg/m2)]) and Fat Mass Index (FMI) [kg/m2)])
were based on body fat percentage, weight, and height. To analyze the associations,
we used linear mixed-effect regression models. Finally, the total cohort was split
into three biologically relevant age groups (cut-off set at <12 years, ≥12
to ≤15 years and >15 years).\r\n \r\n
\ Results\r\n Median
follow-up was 2.1 years. Overall, change toward a later chronotype was significantly
related with an increase in FMI (ß: 0.05, 95% CI: 0.01–0.08). A 1 h increase in
social jetlag predicted an increase in BMI-SDS of 0.08 SDS units (95% CI: 0.01–0.14)
and in FMI of 0.04 kg/m2 (95% CI: 0.003–0.08). Associations were stronger for
the age group ≥12 to ≤15 years (p for interaction:
<0.001). No relationship was found with FFMI.\r\n \r\n
\ Conclusions\r\n Changes
in MSFsc and SJL during adolescence were associated with concurrent changes in
BMI-SDS and FMI. The age ≥12 to ≤15 years appears to be a sensitive period in
which chronobiological changes were clearly associated with increasing body fatness.\r\n
\ "
author:
- first_name: Nicole
full_name: Jankovic, Nicole
last_name: Jankovic
- first_name: Sarah
full_name: Schmitting, Sarah
last_name: Schmitting
- first_name: Bettina
full_name: Krüger, Bettina
id: '49428'
last_name: Krüger
orcid: 0000-0001-5351-1785
- first_name: Ute
full_name: Nöthlings, Ute
last_name: Nöthlings
- first_name: Anette E.
full_name: Buyken, Anette E.
id: '65985'
last_name: Buyken
- first_name: Ute
full_name: Alexy, Ute
last_name: Alexy
citation:
ama: Jankovic N, Schmitting S, Krüger B, Nöthlings U, Buyken AE, Alexy U. Changes
in chronotype and social jetlag during adolescence and their association with
concurrent changes in BMI-SDS and body composition, in the DONALD Study. European
Journal of Clinical Nutrition. Published online 2021. doi:10.1038/s41430-021-01024-y
apa: Jankovic, N., Schmitting, S., Krüger, B., Nöthlings, U., Buyken, A. E., &
Alexy, U. (2021). Changes in chronotype and social jetlag during adolescence and
their association with concurrent changes in BMI-SDS and body composition, in
the DONALD Study. European Journal of Clinical Nutrition. https://doi.org/10.1038/s41430-021-01024-y
bibtex: '@article{Jankovic_Schmitting_Krüger_Nöthlings_Buyken_Alexy_2021, title={Changes
in chronotype and social jetlag during adolescence and their association with
concurrent changes in BMI-SDS and body composition, in the DONALD Study}, DOI={10.1038/s41430-021-01024-y},
journal={European Journal of Clinical Nutrition}, author={Jankovic, Nicole and
Schmitting, Sarah and Krüger, Bettina and Nöthlings, Ute and Buyken, Anette E.
and Alexy, Ute}, year={2021} }'
chicago: Jankovic, Nicole, Sarah Schmitting, Bettina Krüger, Ute Nöthlings, Anette
E. Buyken, and Ute Alexy. “Changes in Chronotype and Social Jetlag during Adolescence
and Their Association with Concurrent Changes in BMI-SDS and Body Composition,
in the DONALD Study.” European Journal of Clinical Nutrition, 2021. https://doi.org/10.1038/s41430-021-01024-y.
ieee: 'N. Jankovic, S. Schmitting, B. Krüger, U. Nöthlings, A. E. Buyken, and U.
Alexy, “Changes in chronotype and social jetlag during adolescence and their association
with concurrent changes in BMI-SDS and body composition, in the DONALD Study,”
European Journal of Clinical Nutrition, 2021, doi: 10.1038/s41430-021-01024-y.'
mla: Jankovic, Nicole, et al. “Changes in Chronotype and Social Jetlag during Adolescence
and Their Association with Concurrent Changes in BMI-SDS and Body Composition,
in the DONALD Study.” European Journal of Clinical Nutrition, 2021, doi:10.1038/s41430-021-01024-y.
short: N. Jankovic, S. Schmitting, B. Krüger, U. Nöthlings, A.E. Buyken, U. Alexy,
European Journal of Clinical Nutrition (2021).
date_created: 2021-11-03T12:57:29Z
date_updated: 2022-01-06T06:57:35Z
department:
- _id: '35'
- _id: '22'
- _id: '571'
doi: 10.1038/s41430-021-01024-y
language:
- iso: eng
publication: European Journal of Clinical Nutrition
publication_identifier:
issn:
- 0954-3007
- 1476-5640
publication_status: published
status: public
title: Changes in chronotype and social jetlag during adolescence and their association
with concurrent changes in BMI-SDS and body composition, in the DONALD Study
type: journal_article
user_id: '49428'
year: '2021'
...
---
_id: '54928'
abstract:
- lang: eng
text: The epithelial Na+ channel (ENaC) is a heteromeric channel composed of three
subunits ($\alpha$, $\beta$, $\gamma$). At the C-terminus of each subunit, a PY-motif
allows binding of the ubiquitin ligase Nedd4-2 which plays a key role in promoting
ENaC retrieval from the plasma membrane. Phosphorylation of Nedd4-2 by the serum
and glucocorticoid-inducible kinase 1 (Sgk1) reduces Nedd4-2 binding to the PY-motifs.
In $\beta$ and $\gamma$ENaC, threonine residues ($\beta$T613, $\gamma$T623) belong
to an extracellular signal-regulated kinase (ERK) motif and directly precede the
PY-motifs. Thus, phosphorylation of these residues may modulate the interaction
of their adjacent PY-motifs with Nedd4-2. In this study, a phosphospecific antibody
was used to demonstrate phosphorylation of $\beta$T613 in Xenopus laevis oocytes
heterologously expressing rat $\alpha$$\beta$$\gamma$ENaC. Treating the oocytes
with progesterone to stimulate ERK increased phosphorylation of $\beta$T613. Inactivation
of the putative phosphorylation sites by mutating both threonine residues to alanine
($\beta$T613A/$\gamma$T623A) increased ENaC-mediated amiloride-sensitive whole-cell
currents ($\Delta$Iami) and expression of $\beta$ENaC at the cell surface. Co-expression
of Nedd4-2 largely reduced $\Delta$Iami in oocytes expressing $\alpha$$\beta$$\gamma$ENaC
or channels with mutated PY-motifs in $\alpha$ and $\gamma$ENaC or in $\alpha$
and $\beta$ENaC. Importantly, the inhibitory effect of co-expressed Nedd4-2 was
largely reduced in channels with mutated PY-motifs in $\alpha$ and $\gamma$ENaC
when combined with the $\beta$T613A mutation but conserved in channels with mutated
PY-motifs in $\alpha$ and $\beta$ENaC combined with the $\gamma$T623A mutation.
These results suggest that phosphorylation and dephosphorylation of $\beta$T613
play a prominent role in regulating Nedd4-2-mediated ENaC retrieval from the plasma
membrane.
author:
- first_name: Bettina
full_name: Krueger, Bettina
id: '49428'
last_name: Krueger
orcid: 0000-0001-5351-1785
- first_name: Limin
full_name: Yang, Limin
last_name: Yang
- first_name: Christoph
full_name: Korbmacher, Christoph
last_name: Korbmacher
- first_name: Robert
full_name: Rauh, Robert
last_name: Rauh
citation:
ama: Krueger B, Yang L, Korbmacher C, Rauh R. The phosphorylation site T613 in the
$\beta$-subunit of rat epithelial Na+ channel (ENaC) modulates channel inhibition
by Nedd4-2. Pflügers Archiv - European Journal of Physiology. 2018;470(4):649–660.
doi:10.1007/s00424-018-2115-2
apa: Krueger, B., Yang, L., Korbmacher, C., & Rauh, R. (2018). The phosphorylation
site T613 in the $\beta$-subunit of rat epithelial Na+ channel (ENaC) modulates
channel inhibition by Nedd4-2. Pflügers Archiv - European Journal of Physiology,
470(4), 649–660. https://doi.org/10.1007/s00424-018-2115-2
bibtex: '@article{Krueger_Yang_Korbmacher_Rauh_2018, title={The phosphorylation
site T613 in the $\beta$-subunit of rat epithelial Na+ channel (ENaC) modulates
channel inhibition by Nedd4-2}, volume={470}, DOI={10.1007/s00424-018-2115-2},
number={4}, journal={Pflügers Archiv - European Journal of Physiology}, publisher={Springer},
author={Krueger, Bettina and Yang, Limin and Korbmacher, Christoph and Rauh, Robert},
year={2018}, pages={649–660} }'
chicago: 'Krueger, Bettina, Limin Yang, Christoph Korbmacher, and Robert Rauh. “The
Phosphorylation Site T613 in the $\beta$-Subunit of Rat Epithelial Na+ Channel
(ENaC) Modulates Channel Inhibition by Nedd4-2.” Pflügers Archiv - European
Journal of Physiology 470, no. 4 (2018): 649–660. https://doi.org/10.1007/s00424-018-2115-2.'
ieee: 'B. Krueger, L. Yang, C. Korbmacher, and R. Rauh, “The phosphorylation site
T613 in the $\beta$-subunit of rat epithelial Na+ channel (ENaC) modulates channel
inhibition by Nedd4-2,” Pflügers Archiv - European Journal of Physiology,
vol. 470, no. 4, pp. 649–660, 2018, doi: 10.1007/s00424-018-2115-2.'
mla: Krueger, Bettina, et al. “The Phosphorylation Site T613 in the $\beta$-Subunit
of Rat Epithelial Na+ Channel (ENaC) Modulates Channel Inhibition by Nedd4-2.”
Pflügers Archiv - European Journal of Physiology, vol. 470, no. 4, Springer,
2018, pp. 649–660, doi:10.1007/s00424-018-2115-2.
short: B. Krueger, L. Yang, C. Korbmacher, R. Rauh, Pflügers Archiv - European Journal
of Physiology 470 (2018) 649–660.
date_created: 2024-06-30T13:43:17Z
date_updated: 2024-06-30T13:43:39Z
department:
- _id: '35'
- _id: '22'
doi: 10.1007/s00424-018-2115-2
intvolume: ' 470'
issue: '4'
language:
- iso: eng
page: 649–660
publication: Pflügers Archiv - European Journal of Physiology
publisher: Springer
status: public
title: The phosphorylation site T613 in the $\beta$-subunit of rat epithelial Na+
channel (ENaC) modulates channel inhibition by Nedd4-2
type: journal_article
user_id: '49428'
volume: 470
year: '2018'
...
---
_id: '54929'
abstract:
- lang: eng
text: The epithelial sodium channel (ENaC) is rate limiting for Na(+) absorption
in the aldosterone-sensitive distal nephron comprising the late distal convoluted
tubule (DCT2), the connecting tubule (CNT), and the entire collecting duct. Liddle
syndrome (pseudohyperaldosteronism), a severe form of salt-sensitive hypertension,
is caused by gain-of-function mutations of ENaC, but the precise tubular site
of increased ENaC function is unknown. In the cortical collecting duct (CCD),
ENaC is known to be regulated by aldosterone. In contrast, we recently reported
aldosterone-independent ENaC regulation in the early part of the aldosterone-sensitive
distal nephron. Here, we investigated ENaC function in the transition zone of
DCT2/CNT or CNT/CCD microdissected from mice homozygous for Liddle syndrome mutation
or from wild-type control mice. Whole-cell patch-clamp recordings were used to
measure amiloride-sensitive ENaC currents in nephron fragments from mice maintained
on different sodium diets to vary plasma aldosterone levels. Our data indicate
that in mice with Liddle syndrome, the primary site of increased Na(+) reabsorption
is the DCT2/CNT. In addition, increased aldosterone responsiveness of ENaC in
CNT/CCD may contribute to salt-sensitive hypertension in Liddle syndrome. Single
channel properties of ENaC were similar in Liddle syndrome mutation and wild-type
mice, but ENaC expression at the apical membrane was increased in Liddle syndrome
mutation when compared with wild-type mice, in particular, in animals maintained
on a high salt diet. Our findings highlight the importance of ENaC function and
regulation in the early part of the aldosterone-sensitive distal nephron for the
maintenance of sodium balance and blood pressure control.
author:
- first_name: Viatcheslav
full_name: Nesterov, Viatcheslav
last_name: Nesterov
- first_name: Bettina
full_name: Krueger, Bettina
id: '49428'
last_name: Krueger
orcid: 0000-0001-5351-1785
- first_name: Marko
full_name: Bertog, Marko
last_name: Bertog
- first_name: Anke
full_name: Dahlmann, Anke
last_name: Dahlmann
- first_name: Ralf
full_name: Palmisano, Ralf
last_name: Palmisano
- first_name: Christoph
full_name: Korbmacher, Christoph
last_name: Korbmacher
citation:
ama: Nesterov V, Krueger B, Bertog M, Dahlmann A, Palmisano R, Korbmacher C. In
Liddle Syndrome, Epithelial Sodium Channel Is Hyperactive Mainly in the Early
Part of the Aldosterone-Sensitive Distal Nephron. Hypertension. 2016;67(6):1256–1262.
doi:10.1161/hypertensionaha.115.07061
apa: Nesterov, V., Krueger, B., Bertog, M., Dahlmann, A., Palmisano, R., & Korbmacher,
C. (2016). In Liddle Syndrome, Epithelial Sodium Channel Is Hyperactive Mainly
in the Early Part of the Aldosterone-Sensitive Distal Nephron. Hypertension,
67(6), 1256–1262. https://doi.org/10.1161/hypertensionaha.115.07061
bibtex: '@article{Nesterov_Krueger_Bertog_Dahlmann_Palmisano_Korbmacher_2016, title={In
Liddle Syndrome, Epithelial Sodium Channel Is Hyperactive Mainly in the Early
Part of the Aldosterone-Sensitive Distal Nephron}, volume={67}, DOI={10.1161/hypertensionaha.115.07061},
number={6}, journal={Hypertension}, publisher={Ovid Technologies (Wolters Kluwer
Health)}, author={Nesterov, Viatcheslav and Krueger, Bettina and Bertog, Marko
and Dahlmann, Anke and Palmisano, Ralf and Korbmacher, Christoph}, year={2016},
pages={1256–1262} }'
chicago: 'Nesterov, Viatcheslav, Bettina Krueger, Marko Bertog, Anke Dahlmann, Ralf
Palmisano, and Christoph Korbmacher. “In Liddle Syndrome, Epithelial Sodium Channel
Is Hyperactive Mainly in the Early Part of the Aldosterone-Sensitive Distal Nephron.”
Hypertension 67, no. 6 (2016): 1256–1262. https://doi.org/10.1161/hypertensionaha.115.07061.'
ieee: 'V. Nesterov, B. Krueger, M. Bertog, A. Dahlmann, R. Palmisano, and C. Korbmacher,
“In Liddle Syndrome, Epithelial Sodium Channel Is Hyperactive Mainly in the Early
Part of the Aldosterone-Sensitive Distal Nephron,” Hypertension, vol. 67,
no. 6, pp. 1256–1262, 2016, doi: 10.1161/hypertensionaha.115.07061.'
mla: Nesterov, Viatcheslav, et al. “In Liddle Syndrome, Epithelial Sodium Channel
Is Hyperactive Mainly in the Early Part of the Aldosterone-Sensitive Distal Nephron.”
Hypertension, vol. 67, no. 6, Ovid Technologies (Wolters Kluwer Health),
2016, pp. 1256–1262, doi:10.1161/hypertensionaha.115.07061.
short: V. Nesterov, B. Krueger, M. Bertog, A. Dahlmann, R. Palmisano, C. Korbmacher,
Hypertension 67 (2016) 1256–1262.
date_created: 2024-06-30T13:44:27Z
date_updated: 2024-06-30T13:44:45Z
department:
- _id: '35'
- _id: '22'
doi: 10.1161/hypertensionaha.115.07061
intvolume: ' 67'
issue: '6'
language:
- iso: eng
page: 1256–1262
publication: Hypertension
publisher: Ovid Technologies (Wolters Kluwer Health)
status: public
title: In Liddle Syndrome, Epithelial Sodium Channel Is Hyperactive Mainly in the
Early Part of the Aldosterone-Sensitive Distal Nephron
type: journal_article
user_id: '49428'
volume: 67
year: '2016'
...
---
_id: '54943'
abstract:
- lang: eng
text: Proteolytic activation is a unique feature of the epithelial sodium channel
(ENaC). However, the underlying molecular mechanisms and the physiologically relevant
proteases remain to be identified. The serine protease trypsin I can activate
ENaC in vitro but is unlikely to be the physiologically relevant activating protease
in ENaC-expressing tissues in vivo. Herein, we investigated whether human trypsin
IV, a form of trypsin that is co-expressed in several extrapancreatic epithelial
cells with ENaC, can activate human ENaC. In Xenopus laevis oocytes, we monitored
proteolytic activation of ENaC currents and the appearance of $\gamma$ENaC cleavage
products at the cell surface. We demonstrated that trypsin IV and trypsin I can
stimulate ENaC heterologously expressed in oocytes. ENaC cleavage and activation
by trypsin IV but not by trypsin I required a critical cleavage site (Lys-189)
in the extracellular domain of the $\gamma$-subunit. In contrast, channel activation
by trypsin I was prevented by mutating three putative cleavage sites (Lys-168,
Lys-170, and Arg-172) in addition to mutating previously described prostasin (RKRK(178)),
plasmin (Lys-189), and neutrophil elastase (Val-182 and Val-193) sites. Moreover,
we found that trypsin IV is expressed in human renal epithelial cells and can
increase ENaC-mediated sodium transport in cultured human airway epithelial cells.
Thus, trypsin IV may regulate ENaC function in epithelial tissues. Our results
show, for the first time, that trypsin IV can stimulate ENaC and that trypsin
IV and trypsin I activate ENaC by cleavage at distinct sites. The presence of
distinct cleavage sites may be important for ENaC regulation by tissue-specific
proteases.
author:
- first_name: Silke
full_name: Haerteis, Silke
last_name: Haerteis
- first_name: Annabel
full_name: Krappitz, Annabel
last_name: Krappitz
- first_name: Matteus
full_name: Krappitz, Matteus
last_name: Krappitz
- first_name: Jane E.
full_name: Murphy, Jane E.
last_name: Murphy
- first_name: Marko
full_name: Bertog, Marko
last_name: Bertog
- first_name: Bettina
full_name: Krueger, Bettina
id: '49428'
last_name: Krueger
orcid: 0000-0001-5351-1785
- first_name: Regina
full_name: Nacken, Regina
last_name: Nacken
- first_name: Hyunjae
full_name: Chung, Hyunjae
last_name: Chung
- first_name: Morley D.
full_name: Hollenberg, Morley D.
last_name: Hollenberg
- first_name: Wolfgang
full_name: Knecht, Wolfgang
last_name: Knecht
- first_name: Nigel W.
full_name: Bunnett, Nigel W.
last_name: Bunnett
- first_name: Christoph
full_name: Korbmacher, Christoph
last_name: Korbmacher
citation:
ama: Haerteis S, Krappitz A, Krappitz M, et al. Proteolytic Activation of the Human
Epithelial Sodium Channel by Trypsin IV and Trypsin I Involves Distinct Cleavage
Sites. Journal of Biological Chemistry. 2014;289(27):19067–19078. doi:10.1074/jbc.m113.538470
apa: Haerteis, S., Krappitz, A., Krappitz, M., Murphy, J. E., Bertog, M., Krueger,
B., Nacken, R., Chung, H., Hollenberg, M. D., Knecht, W., Bunnett, N. W., &
Korbmacher, C. (2014). Proteolytic Activation of the Human Epithelial Sodium Channel
by Trypsin IV and Trypsin I Involves Distinct Cleavage Sites. Journal of Biological
Chemistry, 289(27), 19067–19078. https://doi.org/10.1074/jbc.m113.538470
bibtex: '@article{Haerteis_Krappitz_Krappitz_Murphy_Bertog_Krueger_Nacken_Chung_Hollenberg_Knecht_et
al._2014, title={Proteolytic Activation of the Human Epithelial Sodium Channel
by Trypsin IV and Trypsin I Involves Distinct Cleavage Sites}, volume={289}, DOI={10.1074/jbc.m113.538470}, number={27},
journal={Journal of Biological Chemistry}, publisher={Elsevier}, author={Haerteis,
Silke and Krappitz, Annabel and Krappitz, Matteus and Murphy, Jane E. and Bertog,
Marko and Krueger, Bettina and Nacken, Regina and Chung, Hyunjae and Hollenberg,
Morley D. and Knecht, Wolfgang and et al.}, year={2014}, pages={19067–19078} }'
chicago: 'Haerteis, Silke, Annabel Krappitz, Matteus Krappitz, Jane E. Murphy, Marko
Bertog, Bettina Krueger, Regina Nacken, et al. “Proteolytic Activation of the
Human Epithelial Sodium Channel by Trypsin IV and Trypsin I Involves Distinct
Cleavage Sites.” Journal of Biological Chemistry 289, no. 27 (2014): 19067–19078.
https://doi.org/10.1074/jbc.m113.538470.'
ieee: 'S. Haerteis et al., “Proteolytic Activation of the Human Epithelial
Sodium Channel by Trypsin IV and Trypsin I Involves Distinct Cleavage Sites,”
Journal of Biological Chemistry, vol. 289, no. 27, pp. 19067–19078, 2014,
doi: 10.1074/jbc.m113.538470.'
mla: Haerteis, Silke, et al. “Proteolytic Activation of the Human Epithelial Sodium
Channel by Trypsin IV and Trypsin I Involves Distinct Cleavage Sites.” Journal
of Biological Chemistry, vol. 289, no. 27, Elsevier, 2014, pp. 19067–19078,
doi:10.1074/jbc.m113.538470.
short: S. Haerteis, A. Krappitz, M. Krappitz, J.E. Murphy, M. Bertog, B. Krueger,
R. Nacken, H. Chung, M.D. Hollenberg, W. Knecht, N.W. Bunnett, C. Korbmacher,
Journal of Biological Chemistry 289 (2014) 19067–19078.
date_created: 2024-06-30T13:57:24Z
date_updated: 2024-06-30T13:57:37Z
department:
- _id: '35'
- _id: '22'
doi: 10.1074/jbc.m113.538470
intvolume: ' 289'
issue: '27'
language:
- iso: eng
page: 19067–19078
publication: Journal of Biological Chemistry
publisher: Elsevier
status: public
title: Proteolytic Activation of the Human Epithelial Sodium Channel by Trypsin IV
and Trypsin I Involves Distinct Cleavage Sites
type: journal_article
user_id: '49428'
volume: 289
year: '2014'
...
---
_id: '54933'
abstract:
- lang: eng
text: In some patients with atypical cystic fibrosis (CF), only one allele of the
CF transmembrane conductance regulator (CFTR) gene is affected. Mutations of the
epithelial sodium channel (ENaC) may contribute to the pathophysiology of the
disease in these patients. To functionally characterize a mutation in the $\beta$-subunit
of ENaC ($\beta$V348M) recently identified in a patient with severe CF-like symptoms
(Mutesa et al. 2009), we expressed wild-type (wt) $\alpha$$\beta$$\gamma$ENaC
or mutant $\alpha$$\beta$V348M$\gamma$ENaC in Xenopus laevis oocytes. The $\beta$V348M
mutation stimulated amiloride-sensitive whole-cell current ($\Delta$I(ami)) by
$\sim$40% but had no effect on surface expression or single-channel conductance
of ENaC. Instead the mutation increased channel open probability (P(o)). Proteolytic
activation of mutant ENaC by chymotrypsin was reduced compared with that of wt
ENaC ($\sim$3.0-fold vs. $\sim$4.2-fold), which is consistent with the increased
baseline P(o) of mutant ENaC. Similarly, the ENaC activator S3969 stimulated mutant
ENaC currents to a lesser degree (by $\sim$2.6-fold) than wt ENaC currents (by
$\sim$3.5-fold). The gain-of-function effect of the $\beta$V348M mutation was
confirmed by whole-cell current measurements in HEK293 cells transiently transfected
with wt or mutant ENaC. Computational channel modeling in combination with functional
expression of different $\beta$V348 mutants in oocytes suggests that the $\beta$V348M
mutation increases channel P(o) by destabilizing the closed channel state. Our
findings indicate that the gain-of-function effect of the $\beta$V348M mutation
may contribute to CF pathophysiology by inappropriately increasing sodium and
fluid absorption in the respiratory tract.
author:
- first_name: Robert
full_name: Rauh, Robert
last_name: Rauh
- first_name: Daniel
full_name: Soell, Daniel
last_name: Soell
- first_name: Silke
full_name: Haerteis, Silke
last_name: Haerteis
- first_name: Alexei
full_name: Diakov, Alexei
last_name: Diakov
- first_name: Viatcheslav
full_name: Nesterov, Viatcheslav
last_name: Nesterov
- first_name: Bettina
full_name: Krueger, Bettina
id: '49428'
last_name: Krueger
orcid: 0000-0001-5351-1785
- first_name: Heinrich
full_name: Sticht, Heinrich
last_name: Sticht
- first_name: Christoph
full_name: Korbmacher, Christoph
last_name: Korbmacher
citation:
ama: Rauh R, Soell D, Haerteis S, et al. A mutation in the $\beta$-subunit of ENaC
identified in a patient with cystic fibrosis-like symptoms has a gain-of-function
effect. American Journal of Physiology-Lung Cellular and Molecular Physiology.
2013;304(1):L43–L55. doi:10.1152/ajplung.00093.2012
apa: Rauh, R., Soell, D., Haerteis, S., Diakov, A., Nesterov, V., Krueger, B., Sticht,
H., & Korbmacher, C. (2013). A mutation in the $\beta$-subunit of ENaC identified
in a patient with cystic fibrosis-like symptoms has a gain-of-function effect.
American Journal of Physiology-Lung Cellular and Molecular Physiology,
304(1), L43–L55. https://doi.org/10.1152/ajplung.00093.2012
bibtex: '@article{Rauh_Soell_Haerteis_Diakov_Nesterov_Krueger_Sticht_Korbmacher_2013,
title={A mutation in the $\beta$-subunit of ENaC identified in a patient with
cystic fibrosis-like symptoms has a gain-of-function effect}, volume={304}, DOI={10.1152/ajplung.00093.2012},
number={1}, journal={American Journal of Physiology-Lung Cellular and Molecular
Physiology}, publisher={American Physiological Society}, author={Rauh, Robert
and Soell, Daniel and Haerteis, Silke and Diakov, Alexei and Nesterov, Viatcheslav
and Krueger, Bettina and Sticht, Heinrich and Korbmacher, Christoph}, year={2013},
pages={L43–L55} }'
chicago: 'Rauh, Robert, Daniel Soell, Silke Haerteis, Alexei Diakov, Viatcheslav
Nesterov, Bettina Krueger, Heinrich Sticht, and Christoph Korbmacher. “A Mutation
in the $\beta$-Subunit of ENaC Identified in a Patient with Cystic Fibrosis-like
Symptoms Has a Gain-of-Function Effect.” American Journal of Physiology-Lung
Cellular and Molecular Physiology 304, no. 1 (2013): L43–L55. https://doi.org/10.1152/ajplung.00093.2012.'
ieee: 'R. Rauh et al., “A mutation in the $\beta$-subunit of ENaC identified
in a patient with cystic fibrosis-like symptoms has a gain-of-function effect,”
American Journal of Physiology-Lung Cellular and Molecular Physiology,
vol. 304, no. 1, pp. L43–L55, 2013, doi: 10.1152/ajplung.00093.2012.'
mla: Rauh, Robert, et al. “A Mutation in the $\beta$-Subunit of ENaC Identified
in a Patient with Cystic Fibrosis-like Symptoms Has a Gain-of-Function Effect.”
American Journal of Physiology-Lung Cellular and Molecular Physiology,
vol. 304, no. 1, American Physiological Society, 2013, pp. L43–L55, doi:10.1152/ajplung.00093.2012.
short: R. Rauh, D. Soell, S. Haerteis, A. Diakov, V. Nesterov, B. Krueger, H. Sticht,
C. Korbmacher, American Journal of Physiology-Lung Cellular and Molecular Physiology
304 (2013) L43–L55.
date_created: 2024-06-30T13:47:44Z
date_updated: 2024-06-30T13:47:56Z
department:
- _id: '35'
- _id: '22'
doi: 10.1152/ajplung.00093.2012
intvolume: ' 304'
issue: '1'
language:
- iso: eng
page: L43–L55
publication: American Journal of Physiology-Lung Cellular and Molecular Physiology
publisher: American Physiological Society
status: public
title: A mutation in the $\beta$-subunit of ENaC identified in a patient with cystic
fibrosis-like symptoms has a gain-of-function effect
type: journal_article
user_id: '49428'
volume: 304
year: '2013'
...
---
_id: '54937'
abstract:
- lang: eng
text: 'Purpose: The epithelial sodium channel (ENaC) is typically expressed in sodium-absorbing
epithelia. Several reports suggest that ENaC is also expressed in ocular tissues
and may play a role in aqueous humor secretion and glaucoma. However, the precise
localization of ENaC in the human eye is still unclear. Here, the authors studied
ENaC expression in 12 normal human donor eyes and in six eyes of patients with
glaucoma. Methods: Quantitative real-time PCR was used to investigate the expression
of $\alpha$-, $\beta$-, $\gamma$-, and $\delta$-ENaC transcripts in ocular tissues.
In addition, the authors performed immunohistochemical studies using recently
generated antibodies against human $\beta$- and $\gamma$-ENaC. Results: At the
mRNA level, all four ENaC subunits were found to be expressed in a wide range
of ocular tissues from normal and glaucomatous human eyes, with the cornea, ciliary
body, iris, and retina showing the highest expression levels. At the protein level,
$\beta$- and $\gamma$-ENaC subunits showed distinct distribution patterns and
could be immunolocalized primarily to the cell membranes of epithelial cells of
the cornea and to the conjunctiva, iris, ciliary body, lens, and retinal pigment
epithelium but also to vascular endothelial cells, smooth muscle cells, stromal
cells, and retinal neurons. The authors found no altered mRNA level of any subunit
in glaucomatous eyes. Conclusions: All four ENaC subunits ($\alpha$$\beta$$\gamma$$\delta$)
are expressed in the normal human eye, with distinct localization of subunits
possibly reflecting different functional states of the channel. The (patho-)physiological
roles of ENaC in the various localizations in the eye remain to be determined.'
author:
- first_name: Bettina
full_name: Krueger, Bettina
id: '49428'
last_name: Krueger
orcid: 0000-0001-5351-1785
- first_name: Ursula
full_name: Schlötzer-Schrehardt, Ursula
last_name: Schlötzer-Schrehardt
- first_name: Silke
full_name: Haerteis, Silke
last_name: Haerteis
- first_name: Matthias
full_name: Zenkel, Matthias
last_name: Zenkel
- first_name: Verena E.
full_name: Chankiewitz, Verena E.
last_name: Chankiewitz
- first_name: Kerstin U.
full_name: Amann, Kerstin U.
last_name: Amann
- first_name: Friedrich E.
full_name: Kruse, Friedrich E.
last_name: Kruse
- first_name: Christoph
full_name: Korbmacher, Christoph
last_name: Korbmacher
citation:
ama: Krueger B, Schlötzer-Schrehardt U, Haerteis S, et al. Four Subunits ($\alpha$$\beta$$\gamma$$\delta$)
of the Epithelial Sodium Channel (ENaC) Are Expressed in the Human Eye in Various
Locations. Investigative Opthalmology & Visual Science. 2012;53(2):596–604.
doi:10.1167/iovs.11-8581
apa: Krueger, B., Schlötzer-Schrehardt, U., Haerteis, S., Zenkel, M., Chankiewitz,
V. E., Amann, K. U., Kruse, F. E., & Korbmacher, C. (2012). Four Subunits
($\alpha$$\beta$$\gamma$$\delta$) of the Epithelial Sodium Channel (ENaC) Are
Expressed in the Human Eye in Various Locations. Investigative Opthalmology
& Visual Science, 53(2), 596–604. https://doi.org/10.1167/iovs.11-8581
bibtex: '@article{Krueger_Schlötzer-Schrehardt_Haerteis_Zenkel_Chankiewitz_Amann_Kruse_Korbmacher_2012,
title={Four Subunits ($\alpha$$\beta$$\gamma$$\delta$) of the Epithelial Sodium
Channel (ENaC) Are Expressed in the Human Eye in Various Locations}, volume={53},
DOI={10.1167/iovs.11-8581},
number={2}, journal={Investigative Opthalmology & Visual Science}, publisher={Association
for Research in Vision and Ophthalmology (ARVO)}, author={Krueger, Bettina and
Schlötzer-Schrehardt, Ursula and Haerteis, Silke and Zenkel, Matthias and Chankiewitz,
Verena E. and Amann, Kerstin U. and Kruse, Friedrich E. and Korbmacher, Christoph},
year={2012}, pages={596–604} }'
chicago: 'Krueger, Bettina, Ursula Schlötzer-Schrehardt, Silke Haerteis, Matthias
Zenkel, Verena E. Chankiewitz, Kerstin U. Amann, Friedrich E. Kruse, and Christoph
Korbmacher. “Four Subunits ($\alpha$$\beta$$\gamma$$\delta$) of the Epithelial
Sodium Channel (ENaC) Are Expressed in the Human Eye in Various Locations.” Investigative
Opthalmology & Visual Science 53, no. 2 (2012): 596–604. https://doi.org/10.1167/iovs.11-8581.'
ieee: 'B. Krueger et al., “Four Subunits ($\alpha$$\beta$$\gamma$$\delta$)
of the Epithelial Sodium Channel (ENaC) Are Expressed in the Human Eye in Various
Locations,” Investigative Opthalmology & Visual Science, vol. 53, no.
2, pp. 596–604, 2012, doi: 10.1167/iovs.11-8581.'
mla: Krueger, Bettina, et al. “Four Subunits ($\alpha$$\beta$$\gamma$$\delta$) of
the Epithelial Sodium Channel (ENaC) Are Expressed in the Human Eye in Various
Locations.” Investigative Opthalmology & Visual Science, vol. 53, no.
2, Association for Research in Vision and Ophthalmology (ARVO), 2012, pp. 596–604,
doi:10.1167/iovs.11-8581.
short: B. Krueger, U. Schlötzer-Schrehardt, S. Haerteis, M. Zenkel, V.E. Chankiewitz,
K.U. Amann, F.E. Kruse, C. Korbmacher, Investigative Opthalmology & Visual
Science 53 (2012) 596–604.
date_created: 2024-06-30T13:51:35Z
date_updated: 2024-06-30T13:52:14Z
department:
- _id: '35'
- _id: '22'
doi: 10.1167/iovs.11-8581
intvolume: ' 53'
issue: '2'
language:
- iso: eng
page: 596–604
publication: Investigative Opthalmology & Visual Science
publisher: Association for Research in Vision and Ophthalmology (ARVO)
status: public
title: Four Subunits ($\alpha$$\beta$$\gamma$$\delta$) of the Epithelial Sodium Channel
(ENaC) Are Expressed in the Human Eye in Various Locations
type: journal_article
user_id: '49428'
volume: 53
year: '2012'
...
---
_id: '54930'
abstract:
- lang: eng
text: 'Background: Increased expression of the pro-fibrotic protein connective tissue
growth factor (CTGF) has been detected in injured kidneys and elevated urinary
levels of CTGF are discussed as prognostic marker of chronic kidney disease. There
is evidence that epithelial cells lining the renal tubular system contribute to
uptake and secretion of CTGF. However, the role of different types of tubular
epithelial cells in these processes so far has not been addressed in primary cultures
of human cells. Results: Tubular epithelial cells of proximal and distal origin
were isolated from human kidneys and cultured as polarized cells in insert wells.
The pro-fibrotic stimuli lysophosphatidic acid (LPA) and transforming growth factor
$\beta$ (TGF-$\beta$) were used to induce CTGF secretion.LPA activated CTGF secretion
in proximal tubular cells when applied from either the apical or the basolateral
side as shown by immunocytochemistry. CTGF was secreted exclusively to the apical
side. Signaling pathways activated by LPA included MAP kinase and Rho kinase signaling.
TGF-$\beta$ applied from either side also stimulated CTGF secretion primarily
to the apical side with little basolateral release.Interestingly, TGF-$\beta$
activation induced different signaling pathways depending on the side of TGF-$\beta$
application. Smad signaling was almost exclusively activated from the basolateral
side most prominently in cells of distal origin. Only part of these cells also
synthesized CTGF indicating that Smad activation alone was not sufficient for
CTGF induction. MAP kinases were involved in apical TGF-$\beta$-mediated activation
of CTGF synthesis in proximal cells and a subset of epithelial cells of distal
origin. This subpopulation of distal tubular cells was also able to internalize
recombinant apical CTGF, in addition to proximal cells which were the main cells
to take up exogenous CTGF. Conclusions: Analysis of polarized human primary renal
epithelial cells in a transwell system shows that vectorial secretion of the pro-fibrotic
protein CTGF depends on the cell type, the stimulus and the signaling pathway
activated. In all conditions, CTGF was secreted mainly to the apical side upon
TGF-$\beta$ and LPA treatment and therefore, likely contributes to increased urinary
CTGF levels in vivo. Moreover, CTGF secreted basolaterally may be active as paracrine
pro-fibrotic mediator.'
author:
- first_name: Jonathan
full_name: Zuehlke, Jonathan
last_name: Zuehlke
- first_name: Astrid
full_name: Ebenau, Astrid
last_name: Ebenau
- first_name: Bettina
full_name: Krueger, Bettina
id: '49428'
last_name: Krueger
orcid: 0000-0001-5351-1785
- first_name: Margarete
full_name: Goppelt-Struebe, Margarete
last_name: Goppelt-Struebe
citation:
ama: Zuehlke J, Ebenau A, Krueger B, Goppelt-Struebe M. Vectorial secretion of CTGF
as a cell-type specific response to LPA and TGF-$\beta$ in human tubular epithelial
cells. Cell Communication and Signaling. 2012;10(1). doi:10.1186/1478-811x-10-25
apa: Zuehlke, J., Ebenau, A., Krueger, B., & Goppelt-Struebe, M. (2012). Vectorial
secretion of CTGF as a cell-type specific response to LPA and TGF-$\beta$ in human
tubular epithelial cells. Cell Communication and Signaling, 10(1).
https://doi.org/10.1186/1478-811x-10-25
bibtex: '@article{Zuehlke_Ebenau_Krueger_Goppelt-Struebe_2012, title={Vectorial
secretion of CTGF as a cell-type specific response to LPA and TGF-$\beta$ in human
tubular epithelial cells}, volume={10}, DOI={10.1186/1478-811x-10-25},
number={1}, journal={Cell Communication and Signaling}, publisher={Springer},
author={Zuehlke, Jonathan and Ebenau, Astrid and Krueger, Bettina and Goppelt-Struebe,
Margarete}, year={2012} }'
chicago: Zuehlke, Jonathan, Astrid Ebenau, Bettina Krueger, and Margarete Goppelt-Struebe.
“Vectorial Secretion of CTGF as a Cell-Type Specific Response to LPA and TGF-$\beta$
in Human Tubular Epithelial Cells.” Cell Communication and Signaling 10,
no. 1 (2012). https://doi.org/10.1186/1478-811x-10-25.
ieee: 'J. Zuehlke, A. Ebenau, B. Krueger, and M. Goppelt-Struebe, “Vectorial secretion
of CTGF as a cell-type specific response to LPA and TGF-$\beta$ in human tubular
epithelial cells,” Cell Communication and Signaling, vol. 10, no. 1, 2012,
doi: 10.1186/1478-811x-10-25.'
mla: Zuehlke, Jonathan, et al. “Vectorial Secretion of CTGF as a Cell-Type Specific
Response to LPA and TGF-$\beta$ in Human Tubular Epithelial Cells.” Cell Communication
and Signaling, vol. 10, no. 1, Springer, 2012, doi:10.1186/1478-811x-10-25.
short: J. Zuehlke, A. Ebenau, B. Krueger, M. Goppelt-Struebe, Cell Communication
and Signaling 10 (2012).
date_created: 2024-06-30T13:45:36Z
date_updated: 2024-06-30T13:45:48Z
department:
- _id: '35'
- _id: '22'
doi: 10.1186/1478-811x-10-25
intvolume: ' 10'
issue: '1'
language:
- iso: eng
publication: Cell Communication and Signaling
publisher: Springer
status: public
title: Vectorial secretion of CTGF as a cell-type specific response to LPA and TGF-$\beta$
in human tubular epithelial cells
type: journal_article
user_id: '49428'
volume: 10
year: '2012'
...
---
_id: '54934'
abstract:
- lang: eng
text: Aldosterone is thought to be the main hormone to stimulate the epithelial
sodium channel (ENaC) in the aldosterone-sensitive distal nephron (ASDN) comprising
the late distal convoluted tubule (DCT2), the connecting tubule (CNT) and the
entire collecting duct (CD). There is immunohistochemical evidence for an axial
gradient of ENaC expression along the ASDN with highest expression in the DCT2
and CNT. However, most of our knowledge about renal ENaC function stems from studies
in the cortical collecting duct (CCD). Here we investigated ENaC function in the
transition zone of DCT2/CNT or CNT/CCD microdissected from mice maintained on
different sodium diets to vary plasma aldosterone levels. Single-channel recordings
demonstrated amiloride-sensitive Na(+) channels in DCT2/CNT with biophysical properties
typical for ENaC previously described in CNT/CCD. In animals maintained on a standard
salt diet, the average ENaC-mediated whole cell current ($\Delta$I(ami)) was higher
in DCT2/CNT than in CNT/CCD. A low salt diet increased $\Delta$I(ami) in CNT/CCD
but had little effect on $\Delta$I(ami) in DCT2/CNT. To investigate whether aldosterone
is necessary for ENaC activity in the DCT2/CNT, we used aldosterone synthase knockout
(AS(-/-)) mice that lack aldosterone. In CNT/CCD of AS(-/-) mice, $\Delta$I(ami)
was lower than that in wild-type (WT) animals and was not stimulated by a low
salt diet. In contrast, in DCT2/CNT of AS(-/-) mice, $\Delta$I(ami) was similar
to that in DCT2/CNT of WT animals both on a standard and on a low salt diet. We
conclude that ENaC function in the DCT2/CNT is largely independent of aldosterone
which is in contrast to its known aldosterone sensitivity in CNT/CCD.
author:
- first_name: Viatcheslav
full_name: Nesterov, Viatcheslav
last_name: Nesterov
- first_name: Anke
full_name: Dahlmann, Anke
last_name: Dahlmann
- first_name: Bettina
full_name: Krueger, Bettina
id: '49428'
last_name: Krueger
orcid: 0000-0001-5351-1785
- first_name: Marko
full_name: Bertog, Marko
last_name: Bertog
- first_name: Johannes
full_name: Loffing, Johannes
last_name: Loffing
- first_name: Christoph
full_name: Korbmacher, Christoph
last_name: Korbmacher
citation:
ama: Nesterov V, Dahlmann A, Krueger B, Bertog M, Loffing J, Korbmacher C. Aldosterone-dependent
and -independent regulation of the epithelial sodium channel (ENaC) in mouse distal
nephron. American Journal of Physiology-Renal Physiology. 2012;303(9):F1289–F1299.
doi:10.1152/ajprenal.00247.2012
apa: Nesterov, V., Dahlmann, A., Krueger, B., Bertog, M., Loffing, J., & Korbmacher,
C. (2012). Aldosterone-dependent and -independent regulation of the epithelial
sodium channel (ENaC) in mouse distal nephron. American Journal of Physiology-Renal
Physiology, 303(9), F1289–F1299. https://doi.org/10.1152/ajprenal.00247.2012
bibtex: '@article{Nesterov_Dahlmann_Krueger_Bertog_Loffing_Korbmacher_2012, title={Aldosterone-dependent
and -independent regulation of the epithelial sodium channel (ENaC) in mouse distal
nephron}, volume={303}, DOI={10.1152/ajprenal.00247.2012},
number={9}, journal={American Journal of Physiology-Renal Physiology}, publisher={American
Physiological Society}, author={Nesterov, Viatcheslav and Dahlmann, Anke and Krueger,
Bettina and Bertog, Marko and Loffing, Johannes and Korbmacher, Christoph}, year={2012},
pages={F1289–F1299} }'
chicago: 'Nesterov, Viatcheslav, Anke Dahlmann, Bettina Krueger, Marko Bertog, Johannes
Loffing, and Christoph Korbmacher. “Aldosterone-Dependent and -Independent Regulation
of the Epithelial Sodium Channel (ENaC) in Mouse Distal Nephron.” American
Journal of Physiology-Renal Physiology 303, no. 9 (2012): F1289–F1299. https://doi.org/10.1152/ajprenal.00247.2012.'
ieee: 'V. Nesterov, A. Dahlmann, B. Krueger, M. Bertog, J. Loffing, and C. Korbmacher,
“Aldosterone-dependent and -independent regulation of the epithelial sodium channel
(ENaC) in mouse distal nephron,” American Journal of Physiology-Renal Physiology,
vol. 303, no. 9, pp. F1289–F1299, 2012, doi: 10.1152/ajprenal.00247.2012.'
mla: Nesterov, Viatcheslav, et al. “Aldosterone-Dependent and -Independent Regulation
of the Epithelial Sodium Channel (ENaC) in Mouse Distal Nephron.” American
Journal of Physiology-Renal Physiology, vol. 303, no. 9, American Physiological
Society, 2012, pp. F1289–F1299, doi:10.1152/ajprenal.00247.2012.
short: V. Nesterov, A. Dahlmann, B. Krueger, M. Bertog, J. Loffing, C. Korbmacher,
American Journal of Physiology-Renal Physiology 303 (2012) F1289–F1299.
date_created: 2024-06-30T13:49:18Z
date_updated: 2024-06-30T13:49:30Z
department:
- _id: '35'
- _id: '22'
doi: 10.1152/ajprenal.00247.2012
intvolume: ' 303'
issue: '9'
language:
- iso: eng
page: F1289–F1299
publication: American Journal of Physiology-Renal Physiology
publisher: American Physiological Society
status: public
title: Aldosterone-dependent and -independent regulation of the epithelial sodium
channel (ENaC) in mouse distal nephron
type: journal_article
user_id: '49428'
volume: 303
year: '2012'
...
---
_id: '54939'
abstract:
- lang: eng
text: 'Background: Renal tubular epithelial cells of proximal and distal origin
differ markedly in their physiological functions. Therefore, we hypothesized that
they also differ in their capacity to undergo epithelial to mesenchymal alterations.
Results: We used cultures of freshly isolated primary human tubular cells. To
distinguish cells of different tubular origin we took advantage of the fact that
human proximal epithelial cells uniquely express N-cadherin instead of E-cadherin
as major cell-cell adhesion molecule. To provoke mesenchymal alteration we treated
these cocultures with TGF-$\beta$ for up to 6 days. Within this time period, the
morphology of distal tubular cells was barely altered. In contrast to tubular
cell lines, E-cadherin was not down-regulated by TGF-$\beta$, even though TGF-$\beta$
signal transduction was initiated as demonstrated by nuclear localization of Smad2/3.
Analysis of transcription factors and miRNAs possibly involved in E-cadherin regulation
revealed high levels of miRNAs of the miR200-family, which may contribute to the
stability of E-cadherin expression in human distal tubular epithelial cells. By
contrast, proximal tubular epithelial cells altered their phenotype when treated
with TGF-$\beta$. They became elongated and formed three-dimensional structures.
Rho-kinases were identified as modulators of TGF-$\beta$-induced morphological
alterations. Non-specific inhibition of Rho-kinases resulted in stabilization
of the epithelial phenotype, while partial effects were observed upon downregulation
of Rho-kinase isoforms ROCK1 and ROCK2. The distinct reactivity of proximal and
distal cells was retained when the cells were cultured as polarized cells. Conclusions:
Interference with Rho-kinase signaling provides a target to counteract TGF-$\beta$-mediated
mesenchymal alterations of epithelial cells, particularly in proximal tubular
epithelial cells. Furthermore, primary distal tubular cells differed from cell
lines by their high phenotypic stability which included constant expression of
E-cadherin. Our cell culture system of primary epithelial cells is thus suitable
to understand and modulate cellular remodeling processes of distinct tubular cells
relevant for human renal disease.'
author:
- first_name: Christof
full_name: Keller, Christof
last_name: Keller
- first_name: Sven
full_name: Kroening, Sven
last_name: Kroening
- first_name: Jonathan
full_name: Zuehlke, Jonathan
last_name: Zuehlke
- first_name: Frank
full_name: Kunath, Frank
last_name: Kunath
- first_name: Bettina
full_name: Krueger, Bettina
id: '49428'
last_name: Krueger
orcid: 0000-0001-5351-1785
- first_name: Margarete
full_name: Goppelt-Struebe, Margarete
last_name: Goppelt-Struebe
citation:
ama: Keller C, Kroening S, Zuehlke J, Kunath F, Krueger B, Goppelt-Struebe M. Distinct
Mesenchymal Alterations in N-Cadherin and E-Cadherin Positive Primary Renal Epithelial
Cells. PLOS ONE. 2012;7(8):e43584. doi:10.1371/journal.pone.0043584
apa: Keller, C., Kroening, S., Zuehlke, J., Kunath, F., Krueger, B., & Goppelt-Struebe,
M. (2012). Distinct Mesenchymal Alterations in N-Cadherin and E-Cadherin Positive
Primary Renal Epithelial Cells. PLOS ONE, 7(8), e43584. https://doi.org/10.1371/journal.pone.0043584
bibtex: '@article{Keller_Kroening_Zuehlke_Kunath_Krueger_Goppelt-Struebe_2012, title={Distinct
Mesenchymal Alterations in N-Cadherin and E-Cadherin Positive Primary Renal Epithelial
Cells}, volume={7}, DOI={10.1371/journal.pone.0043584},
number={8}, journal={PLOS ONE}, publisher={Public Library of Science}, author={Keller,
Christof and Kroening, Sven and Zuehlke, Jonathan and Kunath, Frank and Krueger,
Bettina and Goppelt-Struebe, Margarete}, year={2012}, pages={e43584} }'
chicago: 'Keller, Christof, Sven Kroening, Jonathan Zuehlke, Frank Kunath, Bettina
Krueger, and Margarete Goppelt-Struebe. “Distinct Mesenchymal Alterations in N-Cadherin
and E-Cadherin Positive Primary Renal Epithelial Cells.” PLOS ONE 7, no.
8 (2012): e43584. https://doi.org/10.1371/journal.pone.0043584.'
ieee: 'C. Keller, S. Kroening, J. Zuehlke, F. Kunath, B. Krueger, and M. Goppelt-Struebe,
“Distinct Mesenchymal Alterations in N-Cadherin and E-Cadherin Positive Primary
Renal Epithelial Cells,” PLOS ONE, vol. 7, no. 8, p. e43584, 2012, doi:
10.1371/journal.pone.0043584.'
mla: Keller, Christof, et al. “Distinct Mesenchymal Alterations in N-Cadherin and
E-Cadherin Positive Primary Renal Epithelial Cells.” PLOS ONE, vol. 7,
no. 8, Public Library of Science, 2012, p. e43584, doi:10.1371/journal.pone.0043584.
short: C. Keller, S. Kroening, J. Zuehlke, F. Kunath, B. Krueger, M. Goppelt-Struebe,
PLOS ONE 7 (2012) e43584.
date_created: 2024-06-30T13:53:18Z
date_updated: 2024-06-30T13:53:30Z
department:
- _id: '35'
- _id: '22'
doi: 10.1371/journal.pone.0043584
intvolume: ' 7'
issue: '8'
language:
- iso: eng
page: e43584
publication: PLOS ONE
publication_identifier:
issn:
- 1932-6203
publisher: Public Library of Science
status: public
title: Distinct Mesenchymal Alterations in N-Cadherin and E-Cadherin Positive Primary
Renal Epithelial Cells
type: journal_article
user_id: '49428'
volume: 7
year: '2012'
...
---
_id: '54942'
abstract:
- lang: eng
text: Loss-of-function mutations of the epithelial sodium channel (ENaC) may contribute
to pulmonary symptoms resembling those of patients with atypical cystic fibrosis
(CF). Recently, we identified a loss-of-function mutation in the alpha-subunit
of ENaC (alphaF61L) in an atypical CF patient without mutations in CFTR. To investigate
the functional effect of this mutation, we expressed human wild-type alpha beta
gamma-ENaC or mutant alpha(F61L) beta gamma-ENaC in Xenopus laevis oocytes. The
alphaF61L mutation reduced the ENaC mediated whole-cell currents by approximately
90%. In contrast, the mutation decreased channel surface expression only by approximately
40% and did not alter the single-channel conductance. These findings indicate
that the major effect of the mutation is a reduction of the average channel open
probability (P(o)). This was confirmed by experiments using the betaS520C mutant
ENaC which can be converted to a channel with a P(o) of nearly one, and by experiments
using chymotrypsin to proteolytically activate the channel. These experiments
revealed that the mutation reduced the average P(o) of ENaC by approximately 75%.
Na(+) self inhibition of the mutant channel was significantly enhanced, but the
observed effect was too small to account for the large reduction in average channel
P(o). The ENaC-activator S3969 partially rescued the loss-of-function phenotype
of the alphaF61L mutation. We conclude that the alphaF61L mutation may contribute
to respiratory symptoms in atypical CF patients.
author:
- first_name: Regina
full_name: Huber, Regina
last_name: Huber
- first_name: Bettina
full_name: Krueger, Bettina
id: '49428'
last_name: Krueger
orcid: 0000-0001-5351-1785
- first_name: Alexei
full_name: Diakov, Alexei
last_name: Diakov
- first_name: Judit
full_name: Korbmacher, Judit
last_name: Korbmacher
- first_name: Silke
full_name: Haerteis, Silke
last_name: Haerteis
- first_name: Jürgen
full_name: Einsiedel, Jürgen
last_name: Einsiedel
- first_name: Peter
full_name: Gmeiner, Peter
last_name: Gmeiner
- first_name: Abul
full_name: Azad, Abul
last_name: Azad
- first_name: Harry
full_name: Cuppens, Harry
last_name: Cuppens
- first_name: Jean-Jaques
full_name: Cassiman, Jean-Jaques
last_name: Cassiman
- first_name: Christoph
full_name: Korbmacher, Christoph
last_name: Korbmacher
- first_name: Robert
full_name: Rauh, Robert
last_name: Rauh
citation:
ama: Huber R, Krueger B, Diakov A, et al. Functional Characterization of a Partial
Loss-of-Function Mutation of the Epithelial Sodium Channel (ENaC) Associated with
Atypical Cystic Fibrosis. Cellular Physiology and Biochemistry. 2010;25(001):145–158.
doi:10.1159/000272059
apa: Huber, R., Krueger, B., Diakov, A., Korbmacher, J., Haerteis, S., Einsiedel,
J., Gmeiner, P., Azad, A., Cuppens, H., Cassiman, J.-J., Korbmacher, C., &
Rauh, R. (2010). Functional Characterization of a Partial Loss-of-Function Mutation
of the Epithelial Sodium Channel (ENaC) Associated with Atypical Cystic Fibrosis.
Cellular Physiology and Biochemistry, 25(001), 145–158. https://doi.org/10.1159/000272059
bibtex: '@article{Huber_Krueger_Diakov_Korbmacher_Haerteis_Einsiedel_Gmeiner_Azad_Cuppens_Cassiman_et
al._2010, title={Functional Characterization of a Partial Loss-of-Function Mutation
of the Epithelial Sodium Channel (ENaC) Associated with Atypical Cystic Fibrosis},
volume={25}, DOI={10.1159/000272059},
number={001}, journal={Cellular Physiology and Biochemistry}, publisher={S. Karger
AG}, author={Huber, Regina and Krueger, Bettina and Diakov, Alexei and Korbmacher,
Judit and Haerteis, Silke and Einsiedel, Jürgen and Gmeiner, Peter and Azad, Abul
and Cuppens, Harry and Cassiman, Jean-Jaques and et al.}, year={2010}, pages={145–158}
}'
chicago: 'Huber, Regina, Bettina Krueger, Alexei Diakov, Judit Korbmacher, Silke
Haerteis, Jürgen Einsiedel, Peter Gmeiner, et al. “Functional Characterization
of a Partial Loss-of-Function Mutation of the Epithelial Sodium Channel (ENaC)
Associated with Atypical Cystic Fibrosis.” Cellular Physiology and Biochemistry
25, no. 001 (2010): 145–158. https://doi.org/10.1159/000272059.'
ieee: 'R. Huber et al., “Functional Characterization of a Partial Loss-of-Function
Mutation of the Epithelial Sodium Channel (ENaC) Associated with Atypical Cystic
Fibrosis,” Cellular Physiology and Biochemistry, vol. 25, no. 001, pp.
145–158, 2010, doi: 10.1159/000272059.'
mla: Huber, Regina, et al. “Functional Characterization of a Partial Loss-of-Function
Mutation of the Epithelial Sodium Channel (ENaC) Associated with Atypical Cystic
Fibrosis.” Cellular Physiology and Biochemistry, vol. 25, no. 001, S. Karger
AG, 2010, pp. 145–158, doi:10.1159/000272059.
short: R. Huber, B. Krueger, A. Diakov, J. Korbmacher, S. Haerteis, J. Einsiedel,
P. Gmeiner, A. Azad, H. Cuppens, J.-J. Cassiman, C. Korbmacher, R. Rauh, Cellular
Physiology and Biochemistry 25 (2010) 145–158.
date_created: 2024-06-30T13:56:57Z
date_updated: 2024-06-30T13:57:07Z
department:
- _id: '35'
- _id: '22'
doi: 10.1159/000272059
intvolume: ' 25'
issue: '001'
language:
- iso: eng
page: 145–158
publication: Cellular Physiology and Biochemistry
publisher: S. Karger AG
status: public
title: Functional Characterization of a Partial Loss-of-Function Mutation of the Epithelial
Sodium Channel (ENaC) Associated with Atypical Cystic Fibrosis
type: journal_article
user_id: '49428'
volume: 25
year: '2010'
...
---
_id: '54931'
abstract:
- lang: eng
text: Proteinuria and increased renal reabsorption of NaCl characterize the nephrotic
syndrome. Here, we show that protein-rich urine from nephrotic rats and from patients
with nephrotic syndrome activate the epithelial sodium channel (ENaC) in cultured
M-1 mouse collecting duct cells and in Xenopus laevis oocytes heterologously expressing
ENaC. The activation depended on urinary serine protease activity. We identified
plasmin as a urinary serine protease by matrix-assisted laser desorption/ionization
time of-flight mass spectrometry. Purified plasmin activated ENaC currents, and
inhibitors of plasmin abolished urinary protease activity and the ability to activate
ENaC. In nephrotic syndrome, tubular urokinase-type plasminogen activator likely
converts filtered plasminogen to plasmin. Consistent with this, the combined application
of urokinase-type plasminogen activator and plasminogen stimulated amiloride-sensitive
transepithelial sodium transport in M-1 cells and increased amiloride-sensitive
whole-cell currents in Xenopus laevis oocytes heterologously expressing ENaC.
Activation of ENaC by plasmin involved cleavage and release of an inhibitory peptide
from the ENaC gamma subunit ectodomain. These data suggest that a defective glomerular
filtration barrier allows passage of proteolytic enzymes that have the ability
to activate ENaC.
author:
- first_name: Per
full_name: Svenningsen, Per
last_name: Svenningsen
- first_name: Claus
full_name: Bistrup, Claus
last_name: Bistrup
- first_name: Ulla G.
full_name: Friis, Ulla G.
last_name: Friis
- first_name: Marko
full_name: Bertog, Marko
last_name: Bertog
- first_name: Silke
full_name: Haerteis, Silke
last_name: Haerteis
- first_name: Bettina
full_name: Krueger, Bettina
id: '49428'
last_name: Krueger
orcid: 0000-0001-5351-1785
- first_name: Jane
full_name: Stubbe, Jane
last_name: Stubbe
- first_name: Ole Nørregaard
full_name: Jensen, Ole Nørregaard
last_name: Jensen
- first_name: Helle C.
full_name: Thiesson, Helle C.
last_name: Thiesson
- first_name: Torben R.
full_name: Uhrenholt, Torben R.
last_name: Uhrenholt
- first_name: Bente
full_name: Jespersen, Bente
last_name: Jespersen
- first_name: Boye L.
full_name: Jensen, Boye L.
last_name: Jensen
- first_name: Christoph
full_name: Korbmacher, Christoph
last_name: Korbmacher
- first_name: Ole
full_name: Skøtt, Ole
last_name: Skøtt
citation:
ama: Svenningsen P, Bistrup C, Friis UG, et al. Plasmin in Nephrotic Urine Activates
the Epithelial Sodium Channel. Journal of the American Society of Nephrology.
2009;20(2):299–310. doi:10.1681/asn.2008040364
apa: Svenningsen, P., Bistrup, C., Friis, U. G., Bertog, M., Haerteis, S., Krueger,
B., Stubbe, J., Jensen, O. N., Thiesson, H. C., Uhrenholt, T. R., Jespersen, B.,
Jensen, B. L., Korbmacher, C., & Skøtt, O. (2009). Plasmin in Nephrotic Urine
Activates the Epithelial Sodium Channel. Journal of the American Society of
Nephrology, 20(2), 299–310. https://doi.org/10.1681/asn.2008040364
bibtex: '@article{Svenningsen_Bistrup_Friis_Bertog_Haerteis_Krueger_Stubbe_Jensen_Thiesson_Uhrenholt_et
al._2009, title={Plasmin in Nephrotic Urine Activates the Epithelial Sodium Channel},
volume={20}, DOI={10.1681/asn.2008040364},
number={2}, journal={Journal of the American Society of Nephrology}, publisher={Ovid
Technologies (Wolters Kluwer Health)}, author={Svenningsen, Per and Bistrup, Claus
and Friis, Ulla G. and Bertog, Marko and Haerteis, Silke and Krueger, Bettina
and Stubbe, Jane and Jensen, Ole Nørregaard and Thiesson, Helle C. and Uhrenholt,
Torben R. and et al.}, year={2009}, pages={299–310} }'
chicago: 'Svenningsen, Per, Claus Bistrup, Ulla G. Friis, Marko Bertog, Silke Haerteis,
Bettina Krueger, Jane Stubbe, et al. “Plasmin in Nephrotic Urine Activates the
Epithelial Sodium Channel.” Journal of the American Society of Nephrology
20, no. 2 (2009): 299–310. https://doi.org/10.1681/asn.2008040364.'
ieee: 'P. Svenningsen et al., “Plasmin in Nephrotic Urine Activates the Epithelial
Sodium Channel,” Journal of the American Society of Nephrology, vol. 20,
no. 2, pp. 299–310, 2009, doi: 10.1681/asn.2008040364.'
mla: Svenningsen, Per, et al. “Plasmin in Nephrotic Urine Activates the Epithelial
Sodium Channel.” Journal of the American Society of Nephrology, vol. 20,
no. 2, Ovid Technologies (Wolters Kluwer Health), 2009, pp. 299–310, doi:10.1681/asn.2008040364.
short: P. Svenningsen, C. Bistrup, U.G. Friis, M. Bertog, S. Haerteis, B. Krueger,
J. Stubbe, O.N. Jensen, H.C. Thiesson, T.R. Uhrenholt, B. Jespersen, B.L. Jensen,
C. Korbmacher, O. Skøtt, Journal of the American Society of Nephrology 20 (2009)
299–310.
date_created: 2024-06-30T13:46:31Z
date_updated: 2024-06-30T13:46:44Z
department:
- _id: '35'
- _id: '22'
doi: 10.1681/asn.2008040364
intvolume: ' 20'
issue: '2'
language:
- iso: eng
page: 299–310
publication: Journal of the American Society of Nephrology
publisher: Ovid Technologies (Wolters Kluwer Health)
status: public
title: Plasmin in Nephrotic Urine Activates the Epithelial Sodium Channel
type: journal_article
user_id: '49428'
volume: 20
year: '2009'
...
---
_id: '54932'
abstract:
- lang: eng
text: Incubation of microvascular endothelial cells with combretastatin A-4 phosphate
(CA-4P), a microtubule-destabilizing compound that preferentially targets tumor
vessels, altered cell morphology and induced scattering of Golgi stacks. Concomitantly,
CA-4P up-regulated connective tissue growth factor (CTGF/CCN2), a pleiotropic
factor with antiangiogenic properties. In contrast to the effects of other microtubule-targeting
agents such as colchicine or nocodazole, up-regulation of CTGF was only detectable
in sparse cells, which were not embedded in a cell monolayer. Furthermore, CA-4P
induced CTGF expression in endothelial cells, forming tube-like structures on
basement membrane gels. Up-regulation of CTGF by CA-4P was dependent on Rho kinase
signaling and was increased when p42/44 mitogen-activated protein kinase was inhibited.
Additionally, FoxO transcription factors were identified as potent regulators
of CTGF expression in endothelial cells. Activation of FoxO transcription factors
by inhibition of phosphatidylinositol 3-kinase/AKT signaling resulted in a synergistic
increase in CA-4P-mediated CTGF induction. CA-4P-mediated expression of CTGF was
thus potentiated by the inhibition of kinase pathways, which are targets of novel
antineoplastic drugs. Up-regulation of CTGF by low concentrations of CA-4P may
thus occur in newly formed tumor vessels and contribute to the microvessel destabilization
and antiangiogenic effects of CA-4P observed in vivo.
author:
- first_name: Jana
full_name: Samarin, Jana
last_name: Samarin
- first_name: Margot
full_name: Rehm, Margot
last_name: Rehm
- first_name: Bettina
full_name: Krueger, Bettina
id: '49428'
last_name: Krueger
orcid: 0000-0001-5351-1785
- first_name: Jens
full_name: Waschke, Jens
last_name: Waschke
- first_name: Margarete
full_name: Goppelt-Struebe, Margarete
last_name: Goppelt-Struebe
citation:
ama: Samarin J, Rehm M, Krueger B, Waschke J, Goppelt-Struebe M. Up-Regulation of
Connective Tissue Growth Factor in Endothelial Cells by the Microtubule-Destabilizing
Agent Combretastatin A-4. Molecular Cancer Research. 2009;7(2):180–188.
doi:10.1158/1541-7786.mcr-08-0292
apa: Samarin, J., Rehm, M., Krueger, B., Waschke, J., & Goppelt-Struebe, M.
(2009). Up-Regulation of Connective Tissue Growth Factor in Endothelial Cells
by the Microtubule-Destabilizing Agent Combretastatin A-4. Molecular Cancer
Research, 7(2), 180–188. https://doi.org/10.1158/1541-7786.mcr-08-0292
bibtex: '@article{Samarin_Rehm_Krueger_Waschke_Goppelt-Struebe_2009, title={Up-Regulation
of Connective Tissue Growth Factor in Endothelial Cells by the Microtubule-Destabilizing
Agent Combretastatin A-4}, volume={7}, DOI={10.1158/1541-7786.mcr-08-0292},
number={2}, journal={Molecular Cancer Research}, publisher={American Association
for Cancer Research (AACR)}, author={Samarin, Jana and Rehm, Margot and Krueger,
Bettina and Waschke, Jens and Goppelt-Struebe, Margarete}, year={2009}, pages={180–188}
}'
chicago: 'Samarin, Jana, Margot Rehm, Bettina Krueger, Jens Waschke, and Margarete
Goppelt-Struebe. “Up-Regulation of Connective Tissue Growth Factor in Endothelial
Cells by the Microtubule-Destabilizing Agent Combretastatin A-4.” Molecular
Cancer Research 7, no. 2 (2009): 180–188. https://doi.org/10.1158/1541-7786.mcr-08-0292.'
ieee: 'J. Samarin, M. Rehm, B. Krueger, J. Waschke, and M. Goppelt-Struebe, “Up-Regulation
of Connective Tissue Growth Factor in Endothelial Cells by the Microtubule-Destabilizing
Agent Combretastatin A-4,” Molecular Cancer Research, vol. 7, no. 2, pp.
180–188, 2009, doi: 10.1158/1541-7786.mcr-08-0292.'
mla: Samarin, Jana, et al. “Up-Regulation of Connective Tissue Growth Factor in
Endothelial Cells by the Microtubule-Destabilizing Agent Combretastatin A-4.”
Molecular Cancer Research, vol. 7, no. 2, American Association for Cancer
Research (AACR), 2009, pp. 180–188, doi:10.1158/1541-7786.mcr-08-0292.
short: J. Samarin, M. Rehm, B. Krueger, J. Waschke, M. Goppelt-Struebe, Molecular
Cancer Research 7 (2009) 180–188.
date_created: 2024-06-30T13:47:10Z
date_updated: 2024-06-30T13:47:22Z
department:
- _id: '35'
- _id: '22'
doi: 10.1158/1541-7786.mcr-08-0292
intvolume: ' 7'
issue: '2'
language:
- iso: eng
page: 180–188
publication: Molecular Cancer Research
publisher: American Association for Cancer Research (AACR)
status: public
title: Up-Regulation of Connective Tissue Growth Factor in Endothelial Cells by the
Microtubule-Destabilizing Agent Combretastatin A-4
type: journal_article
user_id: '49428'
volume: 7
year: '2009'
...