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The redox-sensitive cation channel TRPM2 modulates phagocyte ROS production and inflammation
Journal article   Peer reviewed

The redox-sensitive cation channel TRPM2 modulates phagocyte ROS production and inflammation

Anke Di, Xiao-Pei Gao, Feng Qian, Takeshi Kawamura, Jin Han, Claudie Hecquet, Richard D. Ye, Stephen M. Vogel and Asrar B. Malik
Nature immunology, Vol.13(1), pp.29-U130
01/01/2012
DOI: 10.1038/ni.2171
PMCID: PMC3242890
PMID: 22101731
url
https://figshare.com/articles/journal_contribution/The_redox_sensitive_cation_channel_TRPM2_modulates_phagocyte_ROS_production_and_inflammation/10779794View
Open Access

Abstract

The NADPH oxidase activity of phagocytes and its generation of reactive oxygen species (ROS) is critical for host defense, but ROS overproduction can also lead to inflammation and tissue injury. Here we report that TRPM2, a nonselective and redox-sensitive cation channel, inhibited ROS production in phagocytic cells and prevented endotoxin-induced lung inflammation in mice. TRPM2-deficient mice challenged with endotoxin (lipopolysaccharide) had an enhanced inflammatory response and diminished survival relative to that of wild-type mice challenged with endotoxin. TRPM2 functioned by dampening NADPH oxidase-mediated ROS production through depolarization of the plasma membrane in phagocytes. As ROS also activate TRPM2, our findings establish a negative feedback mechanism for the inactivation of ROS production through inhibition of the membrane potential-sensitive NADPH oxidase.
Immunology Life Sciences & Biomedicine Science & Technology

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