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The Effects of Cyclosporine on Protein Expression of P53 and Transforming Growth Factor-Beta in Human Renal Tubular Cells

Published online by Cambridge University Press:  02 July 2020

H. Song
Affiliation:
Cardiorenal Molecular Research, Departments of Surgery and Medicine, University of Maryland School of Medicine, Baltimore, MD, 21201
C. Wei
Affiliation:
Cardiorenal Molecular Research, Departments of Surgery and Medicine, University of Maryland School of Medicine, Baltimore, MD, 21201
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Extract

Cyclosporine-A (CsA) is the widely used immunosuppressant drug in renal transplantation. However, the effects of cyclosporine-A are limited by a significant nephrotoxicity. The mechanisms of CsA-induced allograft nephropathy are remaining controversial. Recent study indicated that cellular apoptosis may contribute to the cyclosporine A-mediated cytotoxic action. To date, regarding the effects of cyclosporine A on renal cell apoptosis-related gene expression remain poorly defined. p53 is an important gene in control of renal cell growth and death. Transforming growth factor-beta (TGF-beta) is a multifunctional cytokine that has anti-proliferative as well as fibrogenic properties.

We hypothesized that cyclosporine-A may increase p53 and TGF-β expression in renal tubular cells. These actions of cyclosporine-A may contribute to the cellular apoptosis, fibrosis and CsA-induced nephrotoxicity. Therefore, current study was designed to determine the effects of cyclosporine-A on the p53 and TGF-βl protein expression by immunohistochemical staining (IHCS) in cultured human tubular cells.

Type
Pathology
Copyright
Copyright © Microscopy Society of America

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References

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