ENDOGLIN, A TRANSFORMING GROWTH FACTOR-BETA-BINDING PROTEIN, IS UP-REGULATED IN CHRONIC PROGRESSIVE RENAL-DISEASE

Citation
P. Roychaudhury et al., ENDOGLIN, A TRANSFORMING GROWTH FACTOR-BETA-BINDING PROTEIN, IS UP-REGULATED IN CHRONIC PROGRESSIVE RENAL-DISEASE, Experimental nephrology, 5(1), 1997, pp. 55-60
Citations number
15
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
10187782
Volume
5
Issue
1
Year of publication
1997
Pages
55 - 60
Database
ISI
SICI code
1018-7782(1997)5:1<55:EATGFP>2.0.ZU;2-7
Abstract
Endoglin is a non-signalling receptor for TGF-P. In view of the import ance of transforming growth factor-beta (TGF-beta) in the pathogenesis of renal disease, we have determined the distribution of TGF-beta in human glomerulonephritis. Endoglin was present within the glomerular m esangium and interstitium in normal kidneys. In diseased biopsies, the re was a weak but significant correlation between staining for endogli n in the interstitium and the extent of chronic histological damage (r = 0.3343, p = 0.003). This was supported by division of biopsies into those showing mild damage and those with moderate to severe damage, w here the latter group had significantly increased interstitial stainin g for endoglin (p = 0.0035). However, there was no correlation between mesangial staining for endoglin and specific types of glomerular path ology, such as IgA nephropathy, suggesting that the interstitial expre ssion of endoglin is associated with increased renal damage independen t of the specific type of glomerular lesion which initiates the proces s. There was also a positive correlation between mesangial cell staini ng for endoglin and interstitial endoglin expression (r = 0.3104, p = 0.003), although the former was not independently associated with chro nic histological damage. These data suggest that the response of inter stitial fibroblasts and mesangial cells may be linked in glomeruloneph ritis. Both could contribute to renal scarring by increased binding of TGF-beta which would be independent of the type of initial glomerular damage.