462
Views
17
CrossRef citations to date
0
Altmetric
Research Article

A novel WD-repeat protein, WDR26, inhibits apoptosis of cardiomyocytes induced by oxidative stress

, , , , , , , , & show all
Pages 777-784 | Received 21 Dec 2011, Accepted 20 Mar 2012, Published online: 10 Apr 2012
 

Abstract

WD40 repeat proteins have a variety of functions, such as signal transduction, transcription regulation, cell cycle control, autophagy and apoptosis. WDR26 is a novel protein of WD40 repeat proteins and up-regulated during myocardial cells ischemic preconditioning (IPC) but its role in myocardial cell apoptosis induced by oxidative stress and its subcellular localisation are not clear. So we investigated the subcellular localisation of WDR26 and WDR26 expression in rat myocardial ischaemia-reperfusion injury model and H9c2 cells stimulated by H2O2. The results showed that WDR26 can be located at mitochondria and induced by ischaemia-reperfusion injury and H2O2. Then we examined the effects induced by H2O2 in H9c2 cells WDR26 expression. The results showed that WDR26 expression can inhibit apoptosis induced by H2O2. Further, we demonstrated that WDR26 inhibit cytochrome c release from mitochondria. These founding indicate that WDR26 protects myocardial cells against oxidative stress.

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.