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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Selective expression of TGF-beta2 and TGF-beta3 isoforms in early mesangioproliferative glomerulonephritis.

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.[1]


  1. Selective expression of TGF-beta2 and TGF-beta3 isoforms in early mesangioproliferative glomerulonephritis. Minto, A.W., Wilson, H.M., Rees, A.J., Quigg, R.J., Brown, P.A. Nephron Exp. Nephrol. (2004) [Pubmed]
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