Immunohistochemical analysis of TGF-βand Smad in glomerular damage

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1) Immunohistochemical study of the expression of TGF-β and Smad in glomerular epithelial cells of various glomerular injury models. A mesangial proliferative GN model induced by an anti-Thy 1 antibody, a glomerular epithelial cell injury model induced by Puromycin Aminonucleoside in Wister rats, and a crescentic formation model induced by an anti- GBM antibody in WKY rats were made, and kidneys of the rats were removed and observed. In these models, TGF-β1 remained unchanged, but the expression of β2 and β3 increased in the cytoplasm of glomerular epithelial cells. All the Smads were observed in the cytoplasm of these cells.2) Immunohistochemical study of the expression of TGF- β and Smad in peritoneal sclerotic lesions Sclerosing peritonitis is a complication associated with a long-term CAPD.Localization of TGF-βwas examined in peritoneal biopsy tissues of sclerotic peritonitis using an immunohistochemical method. While TGF-β1, β2 and β3 were stained slightly in some normal peritoneal mesothelial cells, their receptors RI and R2 were stained in all normal peritoneal mesothelial cells. On the other hand, increased staining of TGF-β1, β2 andβ3 in peritoneal mesothelial cells was observed in cases of sclerosing peritonitis. With the expression of β2 and β3 being particularly strong. In the Smad family, which is the intracellular signaling system of TGF-β, Smad 4 was found in the mesothelial cells of normal peritoneum. There were also some mesothelial cells in which expression of the inhibiting type of Smad 6 and Smad 7 could be confirmed. Conclusion : Suppression of the Smad family (the intracellular signaling system of TGF-β) may be effective for suppressing the action of TGF-β and thereby preventing glomerular and peritoneal lesions.