کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10768994 | 1050818 | 2005 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
VEGF induces proliferation, migration, and TGF-β1 expression in mouse glomerular endothelial cells via mitogen-activated protein kinase and phosphatidylinositol 3-kinase
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کلمات کلیدی
MMPAngiogenesis - آنژیوژنزTransforming growth factor-β1 - تبدیل فاکتور رشد β1Proliferation - ترویجEndothelial cells - سلولهای اندوتلیالCytokine - سیتوکینVascular endothelial growth factor - فاکتور رشد اندوتلیال عروقیFibrosis - فیبروز یا فساد الیافMigration - مهاجرتSignal transduction - هدایت سیگنالKidney - کلیه
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
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-β1 mRNA, enhanced TGF-β1 secretion, and bioactivity. VEGF-induced endothelial cell migration and TGF-β1 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.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 334, Issue 4, 9 September 2005, Pages 1049-1060
Journal: Biochemical and Biophysical Research Communications - Volume 334, Issue 4, 9 September 2005, Pages 1049-1060
نویسندگان
Zhao-Dong Li, Jens Peter Bork, Bettina Krueger, Eleonora Patsenker, Anja Schulze-Krebs, Eckhart G. Hahn, Detlef Schuppan,