Summary: The aim of this study was to examine the relationship of basic fibroblast growth factor (FGF‐2) and its receptor (FGF‐R) to tubular proliferation, interstitial fibrosis, glomerular cell proliferation and crescent formation in the development of anti glomerular basement membrane (GBM) glomerulonephrids in the rat. Using new microwave‐based histochemistry techniques, weak constitutive expression of mRNA and protein for FGF‐2 and FGF‐R was evident in tubules and glomeruli of normal rat kidney. Double and triple staining with the proliferating cell nuclear antigen (PCNA) demonstrated that in disease there was focal up‐regulation of FGF‐2 and FGF‐R mRNA and protein expression within proliferating tubules and fibroblast‐like cells in areas of interstitial fibrosis. In contrast, tubules in non‐inflamed areas of kidney showed no change in FGF‐2 and FGF‐R expression or cellular proliferation. In addition, many FGF‐2+PCNA+ and FGF‐R+PCNA+ cells, probably mesangial cells and podocytes, were evident within glomerular segmental proliferative lesions. of particular interest was the observation that many epithelial cells within cellular crescents, inculding proliferating (PCNA+) epithelial cells, strongly expressed both FGF‐2 and FGF‐R. Furthermore, there was strong FGF‐2 and FGF‐R expression by proliferating fibroblast‐like cells within fibrocellular crescents suggesting that FGF‐2 is involved in the formation and fibrotic progression of glomerular crescents. In conclusion, this study provides evidence that increased expression of FGF‐2 and its receptor may participate in the proliferative/fibrotic response in progressive crescentic glomerulonephritis.
|Number of pages||7|
|Publication status||Published - 1 Jan 1995|
- cell proliferation
- fibroblast growth factor
- fibroblast growth factor receptor
- in situ hybridization