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Table of Contents
Vol. 109, No. 1, 2008
Issue release date: June 2008
Section title: Original Paper
Nephron Exp Nephrol 2008;109:e8
(DOI:10.1159/000131892)

Dexamethasone’s Prosurvival Benefits in Podocytes Require Extracellular Signal-Regulated Kinase Phosphorylation

Wada T.a, b · Pippin J.W.a · Nangaku M.b · Shankland S.J.a
aDivision of Nephrology, University of Washington, Seattle, Wash., USA; bDepartment of Nephrology and Endocrinology, University of Tokyo, Tokyo, Japan

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: February 16, 2007
Accepted: March 18, 2008
Published online: May 15, 2008
Issue release date: June 2008

Number of Print Pages: 1
Number of Figures: 10
Number of Tables: 0

ISSN: (Print)
eISSN: 1660-2129 (Online)

For additional information: http://www.karger.com/NEE

Abstract

Background: The reduction in podocyte number is a critical determinant in the development of glomerular diseases. Our recent study demonstrated that glucocorticoids, which are widely used for the treatment of various forms of glomerular injury characterized by proteinuria, protect podocytes from undergoing apoptosis induced by puromycin aminonucleoside (PA). However, the precise mechanisms underlying the beneficial effects of glucocorticoids on podocytes remain to be fully elucidated. Methods: To clarify the role of p53 in apoptosis-inducing factor (AIF) translocation associated with podocyte apoptosis, we performed immunostaining for AIF on cultured mouse podocytes in the presence of the p53 inhibitor pifithrin-α. Extracellular signal-regulated kinase (ERK) phosphorylation in podocytes was measured by Western blot analysis. The role of ERK phosphorylation in podocyte apoptosis was also investigated utilizing MEK1/2 inhibitor U0126. Results: AIF translocation to nuclei was p53 dependent. Furthermore, phosphorylated ERK was reduced in podocytes exposed to PA, and this was prevented by dexamethasone (DEX). Inhibition of ERK phosphorylation by U0126 enhanced podocyte apoptosis induced by PA. Interestingly, when ERK phosphorylation was inhibited, DEX exerted a proapoptotic effect on podocytes, and this effect was also associated with AIF translocation. Our results showed that DEX did not prevent caspase-3-dependent podocyte apoptosis induced by transforming growth factor-β1 (TGF-β1) or UV-C. Conclusion: These results suggest that ERK phosphorylation and the subcellular localization of AIF are important determinants in the protective effect of DEX in podocytes.

© 2008 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: February 16, 2007
Accepted: March 18, 2008
Published online: May 15, 2008
Issue release date: June 2008

Number of Print Pages: 1
Number of Figures: 10
Number of Tables: 0

ISSN: (Print)
eISSN: 1660-2129 (Online)

For additional information: http://www.karger.com/NEE


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Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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