Localization of fibroblast growth factor-2 (basic FGF) and FGF receptor-1 in adult human kidney

Citation
J. Floege et al., Localization of fibroblast growth factor-2 (basic FGF) and FGF receptor-1 in adult human kidney, KIDNEY INT, 56(3), 1999, pp. 883-897
Citations number
52
Categorie Soggetti
Urology & Nephrology","da verificare
Journal title
KIDNEY INTERNATIONAL
ISSN journal
00852538 → ACNP
Volume
56
Issue
3
Year of publication
1999
Pages
883 - 897
Database
ISI
SICI code
0085-2538(199909)56:3<883:LOFGF(>2.0.ZU;2-T
Abstract
Background. The expression pattern of fibroblast growth factor-2 (FGF-2; ba sic FGF), a pleiotrophic growth factor, as well as one of its receptors (FG FR1), in the kidney is highly controversial. Methods. Using an approach that combines multiple antibodies for immunohist ochemistry and correlative in situ hybridization, we assessed the intrarena l expression of both FGF-2 and FGFR1 in 13 specimens of adult kidney remove d during tumor nephrectomy. Results. The FGF-2 expression pattern in the kidneys as detected by immunoh istochemistry was variable and depended on the antibody used. The most cons istent expression of FGF-2 protein was demonstrated in glomerular parietal epithelial cells, tubular cells (mainly of the distal nephron), as well as arterial endothelial cells. These locations also corresponded to areas of F GF-2 mRNA expression. Additionally, by immunohistochemistry, FGF-2 protein was detected in arterial smooth muscle cells and occasional podocytes. The expression of FGFR1 protein and mRNA was most consistently present in tubul ar cells of the distal nephron and in vascular smooth muscle cells. In situ hybridization, but not immunohistochemistry, also suggested FGFR1 expressi on in cells that could not be precisely identified within the glomerular tu ft as well as some interstitial cells. Conclusion. These data suggest potential autocrine and paracrine pathways w ithin the FGF-2 system, particularly within the vascular walls and in the d istal nephron, and thereby provide information for further mechanistic unde rstanding of the role of the FGF-2 system in human renal disease.