Selective Expression of TGF-β2 and TGF-β3 Isoforms in Early Mesangioproliferative Glomerulonephritis

Abstract

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-β2 and TGF-β3 are less clear. The purpose of this study was to define the temporal expression and abundance of TGF-β 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-β1, TGF-β2, and TGF-β3 revealed distinct differences in normal and nephritic rats. No changes in TGF-β1 staining were observed within glomeruli of either model. In marked contrast, in the one-shot model, TGF-β2 and TGF-β3 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-β1, may be the result of an interplay between individual TGF-β isoforms.

The Role of Regional Posterior Frontal Dura Mater in the Overlying Suture Morphology

“…The TGF-␤1, TGF-␤2, and TGF-␤3 primary antibodies obtained have been shown previously to be specific and possess no crossreactivity for the individual TGF-␤ isoforms in the rat species. 15,16 Tissue sections were deparaffinized and rehydrated in graded ethanol. Endogenous peroxide activity was quenched with 3% hydrogen peroxide in phosphate-buffered saline for 5 minutes, followed by three washes in phosphatebuffered saline.…”

Inhibition of NF-κB-dependent Bcl-xL expression by clusterin promotes albumin-induced tubular cell apoptosis

“…Groups of two mice were killed at weekly intervals, with kidneys evaluated for apoptosis and expression of clusterin, fibroblasts (monoclonal antibody ER/ TR7 59 ), and HSP-47 as a marker for increased collagen synthesis. 41 Kidneys were processed and stained using previously described methods, 60,61 which will be briefly described. Immunohistochemical staining for clusterin (b-chain specific, Santa Cruz Biotechnology, Santa Cruz, CA, USA) was conducted using a Vectastain Elite ABC kit (Vector Laboratories, Burlingame, CA, USA) with some modifications.…”

Induction and Coexpression of Latent Transforming Growth Factor β-Binding Protein-1 and Fibrillin-1 in Experimental Glomerulonephritis

“…In earlier studies, we have shown that glomerular mesangial cells express and secrete both LTBP-1 and fibrillin-1 in vitro [6]. Further, we and others have demonstrated an induction of TGF-β isoforms during experimental anti-Thy1.1 glomerulonephritis, which is characterized by transient mesangial hypercellularity and mesangial matrix expansion [7, 8]. We hypothesized that LTBP-1 and fibrillin-1 are coexpressed in the mesangial matrix and are upregulated during acute anti-Thy1.1 glomerulonephritis.…”