Augmentation of kidney injury by basic fibroblast growth factor or platelet-derived growth factor does not induce progressive diabetic nephropathy in the Goto Kakizaki model of non-insulin-dependent diabetes

1999 ◽  
Vol 134 (3) ◽  
pp. 304-312 ◽  
Author(s):  
Stephen G. Riley ◽  
Robert Steadman ◽  
John D. Williams ◽  
Jürgen Floege ◽  
Aled O. Phillips
Keyword(s):  
Diabetic Nephropathy ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Kidney Injury ◽  
Insulin Dependent Diabetes ◽  
Platelet Derived Growth Factor ◽  
Fibroblast Growth ◽  
Insulin Dependent

scholarly journals Sequential Delivery of Basic Fibroblast Growth Factor and Platelet-Derived Growth Factor for Angiogenesis

2011 ◽  
Vol 17 (9-10) ◽  
pp. 1181-1189 ◽  
Author(s):  
Jillian E. Tengood ◽  
Ryan Ridenour ◽  
Ross Brodsky ◽  
Alan J. Russell ◽  
Steven R. Little
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Platelet Derived Growth Factor ◽  
Fibroblast Growth

Platelet-derived growth factor inhibits basic fibroblast growth factor angiogenic properties in vitro and in vivo through its α receptor

Blood ◽  
2002 ◽  
Vol 99 (6) ◽  
pp. 2045-2053 ◽  
Author(s):  
Francesco De Marchis ◽  
Domenico Ribatti ◽  
Claudia Giampietri ◽  
Alessandro Lentini ◽  
Debora Faraone ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Cell Function ◽  
Dominant Negative ◽  
Mitogen Activated Protein Kinase ◽  
Platelet Derived Growth Factor ◽  
Fibroblast Growth

Abstract Basic fibroblast growth factor (bFGF) and platelet-derived growth factor-BB (PDGF-BB) modulate vascular wall cell function in vitro and angiogenesis in vivo. The aim of the current study was to determine how bovine aorta endothelial cells (BAECs) respond to the simultaneous exposure to PDGF-BB and bFGF. It was found that bFGF-dependent BAEC migration, proliferation, and differentiation into tubelike structures on reconstituted extracellular matrix (Matrigel) were inhibited by PDGF-BB. The role played by PDGF receptor α (PDGF-Rα) was investigated by selective stimulation with PDGF-AA, by blocking PDGF-BB-binding to PDGF-Rα with neomycin, or by transfecting cells with dominant-negative forms of the receptors to selectively impair either PDGF-Rα or PDGF-Rβ function. In all cases, PDGF-Rα impairment abolished the inhibitory effect of PDGF-BB on bFGF-directed BAEC migration. In addition, PDGF-Rα phosphorylation was increased in the presence of bFGF and PDGF, as compared to PDGF alone, whereas mitogen-activated protein kinase phosphorylation was decreased in the presence of PDGF-BB and bFGF compared with bFGF alone. In vivo experiments showed that PDGF-BB and PDGF-AA inhibited bFGF-induced angiogenesis in vivo in the chick embryo chorioallantoic membrane assay and that PDGF-BB inhibited bFGF-induced angiogenesis in Matrigel plugs injected subcutaneously in CD1 mice. Taken together these results show that PDGF inhibits the angiogenic properties of bFGF in vitro and in vivo, likely through PDGF-Rα stimulation.

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