Article ID Journal Published Year Pages File Type
4256142 Transplantation Proceedings 2013 5 Pages PDF
Abstract

Apoptosis, which is usually a response to the microenvironment, requires inactivation of prosurvival molecules. Apoptosis contributes to loss of podocytes in the course of renal injury, an event closely associated with the development of proteinuria. Dexamethasone (DEX) is the standard of care for most forms of nephrotic syndrome. However, the precise mechanisms of DEX action on podocytes are unknown. This study examined the hypothesis that cultured podocytes exposed to puromycin aminonucleoside (PAN) showed a reduced rate of apoptosis upon DEX exposure. Apoptotic podocytes seemed to be related to increased Bad mRNA and protein expressions. DEX reduced apoptosis by decreasing Bad mRNA and protein expressions, thereby protecting podocytes. These findings provided insights into the beneficial effects of DEX directly on podocytes. The present study illustrated the signal transduction mechanism of podocyte apoptosis induced by PAN.

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