Thromb Haemost 2009; 101(04): 619-625
DOI: 10.1160/TH08-10-0641
Theme Issue Article
Schattauer GmbH

Role of H2O2-activated TRPM2 calcium channel in oxidant-induced endothelial injury

Claudie M. Hecquet
1   Department of Pharmacology and Center for Lung and Vascular Biology, University of Illinois College of Medicine, Chicago, Illinois, USA
,
Asrar B. Malik
1   Department of Pharmacology and Center for Lung and Vascular Biology, University of Illinois College of Medicine, Chicago, Illinois, USA
› Author Affiliations
Further Information

Publication History

Received: 05 October 2008

Accepted after minor revision: 18 March 2008

Publication Date:
23 November 2017 (online)

Summary

The transient receptor potential (melastatin) 2 (TRPM2), is an oxidant-activated non-selective cation channel that is widely expressed in mammalian tissues including the vascular endothelium. Oxidative stress, through the generation of oxygen meta-bolites including H2O2, stimulates intracellular ADP-ribose formation which, in turn, opens TRPM2 channels. These channels act as an endogenous redox sensor for mediating oxidative stress/ROS-induced Ca2+ entry and the subsequent specific Ca2+-dependent cellular reactions such as endothelial hyper-permeability and apoptosis. This review summarizes recent findings on the mechanism by which oxidants induce TRPM2 activation, the role of these channels in the signalling vascular endothelial dysfunctions, and the modulation of oxidant-induced TRPM2 activation by PKCα and phospho-tyrosine phosphates L1.

 
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