175
Views
37
CrossRef citations to date
0
Altmetric
Original

Regulation of Bcl-2 phosphorylation in response to oxidative stress in cardiac myocytes

, , &
Pages 809-816 | Received 22 Feb 2009, Published online: 01 Sep 2009
 

Abstract

Oxidative stress promotes cardiac myocyte death and has been implicated in the pathogenesis of many cardiovascular diseases. Bcl-2 family proteins are key regulators of the apoptotic response, while their functions can be regulated by post-transcriptional modifications including phosphorylation, dimerization or proteolytic cleavage. This study used adult cardiac myocytes to test the hypothesis that activation of specific kinase signalling pathways by oxidative stress may modulate either the expression or the phosphorylation of Bcl-2, with the resulting effect of a decrease or increase in its anti-apoptotic function. Stimulation of cardiac myocytes with 0.2 mM H2O2, which induces apoptosis, resulted in a marked down-regulation of Bcl-2 protein simultaneously with an increase in its phosphorylation. Inhibition of p38-MAPK resulted in attenuation of Bcl-2 phosphorylation, whereas inhibition of ERK1/2, JNKs or PI-3-K had no effect. These data suggest that activation of p38 MAPK by oxidative stress results in the phosphorylation and degradation of Bcl-2 and the inactivation of its anti-apoptotic activity.

Log in via your institution

Log in to Taylor & Francis Online

PDF download + Online access

  • 48 hours access to article PDF & online version
  • Article PDF can be downloaded
  • Article PDF can be printed
USD 61.00 Add to cart

Issue Purchase

  • 30 days online access to complete issue
  • Article PDFs can be downloaded
  • Article PDFs can be printed
USD 940.00 Add to cart

* Local tax will be added as applicable

Related Research

People also read lists articles that other readers of this article have read.

Recommended articles lists articles that we recommend and is powered by our AI driven recommendation engine.

Cited by lists all citing articles based on Crossref citations.
Articles with the Crossref icon will open in a new tab.