Intervention by retinoic acid in oxidative stress-induced apoptosis

Nephrol Dial Transplant. 2002:17 Suppl 9:84-7. doi: 10.1093/ndt/17.suppl_9.84.

Abstract

Retinoic acid (RA) has been considered a pro-apoptotic agent, and little is known about its anti-apoptotic potential. In this article, we describe that RA strongly inhibits hydrogen peroxide (H(2)O(2))-induced apoptosis of mesangial cells by intervention in activator protein 1 (AP-1). Our data showed that: (i) H(2)O(2) induces apoptosis of mesangial cells via the AP-1 pathway; (iii) activation of AP-1 by H(2)O(2) is mediated by the c-Jun N-terminal kinase (JNK)-c-Jun/AP-1 pathway and the extracellular signal-regulated kinase-c-Fos/AP-1 pathway; (iii) RA inhibits H(2)O(2)-induced apoptosis via suppression of c-fos/c-jun expression and JNK activation; and (iv) the anti-apoptotic effect of RA is, at least in part, mediated by induction of mitogen-activated protein kinase phosphatase 1.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Apoptosis / physiology*
  • Glomerular Mesangium / cytology
  • Glomerular Mesangium / drug effects
  • Glomerular Mesangium / physiology
  • Humans
  • Hydrogen Peroxide / pharmacology
  • Oxidants / pharmacology
  • Oxidative Stress / physiology*
  • Transcription Factor AP-1 / physiology
  • Tretinoin / pharmacology*

Substances

  • Oxidants
  • Transcription Factor AP-1
  • Tretinoin
  • Hydrogen Peroxide