Background/Aim: Evidence from ex vivo glomerular analysis has implicated overexpression of transforming growth factor (TGF) beta 1 in progressive renal disease. The roles of TGF-beta2 and TGF-beta3 are less clear. The purpose of this study was to define the temporal expression and abundance of TGF-beta isoforms in both acute and progressive Thy-1 glomerulonephritis during the crucial initiation phase of these models. Methods: Acute Thy-1 glomerulonephritis was induced by a single injection of OX7, while the progressive model was induced by two injections, 7 days apart. Results: Cellular infiltration of glomeruli consisted of transient increases of neutrophils and ED1+ macrophages. The distribution of TGF-beta1, TGF-beta2, and TGF-beta3 revealed distinct differences in normal and nephritic rats. No changes in TGF-beta1 staining were observed within glomeruli of either model. In marked contrast, in the one-shot model, TGF-beta2 and TGF-beta3 stainings increased rapidly, yet transiently, throughout affected glomeruli, followed by more sustained staining in glomerular epithelial cells. Diffuse, transient staining was absent in two-shot glomerulonephritis, but an increase in epithelial cell staining mirrored that seen in the one-shot model. Conclusion: Based on these results, we propose that the effects, formerly thought of as solely due to a single entity, TGF-beta1, may be the result of an interplay between individual TGF-beta isoforms. Copyright (C) 2004 S. Karger AG, Basel.
- TGF-beta isoforms
- Thy-1 nephritis
- mesangioproliferative glomerulonephritis
- kidney fibrosis