scholarly journals miR-372-3p is a potential diagnostic factor for diabetic nephropathy and modulates high glucose-induced glomerular endothelial cell dysfunction via targeting fibroblast growth factor-16

2019 ◽  
Author(s):  
Zhiyun Meng ◽  
Fangyuan Li ◽  
Bin Wang
Keyword(s):  
Diabetic Nephropathy ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
High Glucose ◽  
Fibroblast Growth ◽  
Endothelial Cell Dysfunction ◽  
Glomerular Endothelial Cell ◽  
Cell Dysfunction

Role of basic fibroblast growth factor (FGF-2) in diabetic nephropathy and mechanisms of its induction by hyperglycemia in human renal fibroblasts

2009 ◽  
Vol 296 (6) ◽  
pp. F1452-F1463 ◽  
Author(s):  
Radovan Vasko ◽  
Michael Koziolek ◽  
Masami Ikehata ◽  
Maria Pia Rastaldi ◽  
Klaus Jung ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
High Glucose ◽  
Mitogen Activated Protein Kinase ◽  
Fibroblast Growth ◽  
Molecular Signaling

Basic fibroblast growth factor (FGF-2) plays a role in renal fibrogenesis, although its potential implications for tubulointerstitial involvement in diabetic nephropathy are unknown. We evaluated the expression of FGF-2 in kidney biopsies from patients with diabetic nephropathy and studied the mechanisms of its induction in human renal fibroblasts under hyperglycemia. Tubulointerstitial expression of FGF-2 was significantly upregulated in diabetic nephropathy compared with control kidneys with a good correlation to the degree of the injury. Fibroblasts cultivated in high glucose displayed increased FGF-2 mRNA as well as protein synthesis and secretion compared with normal glucose. Proliferation rates under hyperglycemia were significantly higher and could be almost completely inhibited by addition of a neutralizing FGF-2 antibody. Alterations in proliferation were associated with changes in p27kip1 expression. Hyperglycemia induced the expression of PKC-β1 and PKC-β2; however, only inhibition of PKC-β1 but not PKC-β2 led to a significant decrease of FGF-2 levels. Relevance of the culture findings and functional association was corroborated by colocalization of FGF-2 and PKC-β in human diabetic kidneys in vivo. High glucose stimulated fibronectin synthesis and secretion, which could be substantially prevented by inhibition of PKC-β1 and to a lesser extent by inhibiting the FGF-2. Expression of active phosphorylated form of p38 mitogen-activated protein kinase was upregulated under hyperglycemia; however, its inhibition had no effects on FGF-2 synthesis. Our results implicate a role of FGF-2 in high glucose-altered molecular signaling in pathogenesis of diabetic renal disease.

scholarly journals Reduction of cellular stress is essential for Fibroblast growth factor 1 treatment for diabetic nephropathy

2018 ◽  
Vol 22 (12) ◽  
pp. 6294-6303 ◽  
Author(s):  
Yanqing Wu ◽  
Yiyang Li ◽  
Ting Jiang ◽  
Yuan Yuan ◽  
Rui Li ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Cellular Stress ◽  
Fibroblast Growth

scholarly journals Caveolin-1 orchestrates fibroblast growth factor 2 signaling control of angiogenesis in placental artery endothelial cell caveolae

2012 ◽  
Vol 227 (6) ◽  
pp. 2480-2491 ◽  
Author(s):  
Lin Feng ◽  
Wu-Xiang Liao ◽  
Quan Luo ◽  
Hong-Hai Zhang ◽  
Wen Wang ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Caveolin 1
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