VEGF induces proliferation, migration, and TGF-$\beta$1 expression in mouse glomerular endothelial cells via mitogen-activated protein kinase and phosphatidylinositol 3-kinase
Z.-D. Li, J.P. Bork, B. Krueger, E. Patsenker, A. Schulze-Krebs, E.G. Hahn, D. Schuppan, Biochemical and Biophysical Research Communications 334 (2005) 1049–1060.
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Journal Article
| English
Author
Li, Zhao-Dong;
Bork, Jens Peter;
Krueger, BettinaLibreCat ;
Patsenker, Eleonora;
Schulze-Krebs, Anja;
Hahn, Eckhart G.;
Schuppan, Detlef
Abstract
The role of glomerular endothelial cells in kidney fibrosis remains incompletely understood. While endothelia are indispensable for repair of acute damage, they can produce extracellular matrix proteins and profibrogenic cytokines that promote fibrogenesis. We used a murine cell line with all features of glomerular endothelial cells (glEND.2), which dissected the effects of vascular endothelial growth factor (VEGF) on cell migration, proliferation, and profibrogenic cytokine production. VEGF dose-dependently induced glEND.2 cell migration and proliferation, accompanied by up-regulation of VEGFR-2 phosphorylation and mRNA expression. VEGF induced a profibrogenic gene expression profile, including up-regulation of TGF-beta1 mRNA, enhanced TGF-beta1 secretion, and bioactivity. VEGF-induced endothelial cell migration and TGF-beta1 induction were mediated by the phosphatidyl-inositol-3 kinase pathway, while proliferation was dependent on the Erk1/2 MAP kinase pathway. This suggests that differential modulation of glomerular angiogenesis by selective inhibition of the two identified VEGF-induced signaling pathways could be a therapeutic approach to treat kidney fibrosis.
Publishing Year
Journal Title
Biochemical and Biophysical Research Communications
Volume
334
Issue
4
Page
1049–1060
LibreCat-ID
Cite this
Li Z-D, Bork JP, Krueger B, et al. VEGF induces proliferation, migration, and TGF-$\beta$1 expression in mouse glomerular endothelial cells via mitogen-activated protein kinase and phosphatidylinositol 3-kinase. Biochemical and Biophysical Research Communications. 2005;334(4):1049–1060. doi:10.1016/j.bbrc.2005.07.005
Li, Z.-D., Bork, J. P., Krueger, B., Patsenker, E., Schulze-Krebs, A., Hahn, E. G., & Schuppan, D. (2005). VEGF induces proliferation, migration, and TGF-$\beta$1 expression in mouse glomerular endothelial cells via mitogen-activated protein kinase and phosphatidylinositol 3-kinase. Biochemical and Biophysical Research Communications, 334(4), 1049–1060. https://doi.org/10.1016/j.bbrc.2005.07.005
@article{Li_Bork_Krueger_Patsenker_Schulze-Krebs_Hahn_Schuppan_2005, title={VEGF induces proliferation, migration, and TGF-$\beta$1 expression in mouse glomerular endothelial cells via mitogen-activated protein kinase and phosphatidylinositol 3-kinase}, volume={334}, DOI={10.1016/j.bbrc.2005.07.005}, number={4}, journal={Biochemical and Biophysical Research Communications}, publisher={Elsevier}, author={Li, Zhao-Dong and Bork, Jens Peter and Krueger, Bettina and Patsenker, Eleonora and Schulze-Krebs, Anja and Hahn, Eckhart G. and Schuppan, Detlef}, year={2005}, pages={1049–1060} }
Li, Zhao-Dong, Jens Peter Bork, Bettina Krueger, Eleonora Patsenker, Anja Schulze-Krebs, Eckhart G. Hahn, and Detlef Schuppan. “VEGF Induces Proliferation, Migration, and TGF-$\beta$1 Expression in Mouse Glomerular Endothelial Cells via Mitogen-Activated Protein Kinase and Phosphatidylinositol 3-Kinase.” Biochemical and Biophysical Research Communications 334, no. 4 (2005): 1049–1060. https://doi.org/10.1016/j.bbrc.2005.07.005.
Z.-D. Li et al., “VEGF induces proliferation, migration, and TGF-$\beta$1 expression in mouse glomerular endothelial cells via mitogen-activated protein kinase and phosphatidylinositol 3-kinase,” Biochemical and Biophysical Research Communications, vol. 334, no. 4, pp. 1049–1060, 2005, doi: 10.1016/j.bbrc.2005.07.005.
Li, Zhao-Dong, et al. “VEGF Induces Proliferation, Migration, and TGF-$\beta$1 Expression in Mouse Glomerular Endothelial Cells via Mitogen-Activated Protein Kinase and Phosphatidylinositol 3-Kinase.” Biochemical and Biophysical Research Communications, vol. 334, no. 4, Elsevier, 2005, pp. 1049–1060, doi:10.1016/j.bbrc.2005.07.005.