Korean J Pathol.
2000 Sep;34(9):642-651.
Expression of Transforming Growth Factor-beta1 in Cyclosporine-Induced Nephropathy in Rats
- Affiliations
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- 1Departments of Pathology, Keimyung University School of Medicine, Taegu 700-712, Korea
- 2Departments of Internal Medicine, Keimyung University School of Medicine, Taegu 700-712, Korea
Abstract
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Cyclosporine nephropathy was induced by intraperitoneal injection of cyclosporine
25 mg/kg in Sprague-Dawley rats daily for 1, 4, 8, and 12 weeks to clarify the
relationship between cyclosporine nephropathy and the expression of TGF-beta1 with
extracellular matrix deposition. On light microscopic examination, the kidneys in the 12
week cyclosporine-treated rats showed focal or striped fibrosis, vacuolization of tubular
cells, and injury of endothelial cells. Immunohistochemically, TGF-beta1 protein was
strongly expressed in the cyclosporine-treated rat kidneys, especially in the glomerular
endothelial cells, interstitial endothelial cells, tubular epithelial cells, and parietal cells in
the Bowman's capsule of the glomerulus as well as the periglomerular arterioles. The
amount of TGF-beta1 expression was correlated with the morphological change in the
cyclosporine-treated rats. Extracellular matrix, such as fibronectin and collagen IV, was
also expressed in the endothelial cells of the glomerulus and the interstitium. It can be
concluded, therefore that TGF-beta1 protein is probably involved in the early stage of
fibrogenesis in cyclosporine nephropathy. It can be postulated that cyclosporine
nephropathy results from the accumulation of extracellular matrix associated with the
increase of TGF-beta1 transcription. Therefore, these results could be used in reducing
fibrosis in cyclosporine nephropathy.