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10.1038/ni.2171 http://scihub22266oqcxt.onion/10.1038/ni.2171 22101731!3242890!22101731     free     free     free       Nat+Immunol 2011 ; 13 (1): 29-34 Nephropedia Template TP {{tp|p=22101731|t=2011. The redox-sensitive cation channel TRPM2 modulates phagocyte ROS production and inflammation |pdf=|usr=}}{{22101731}} gab.com Text The redox-sensitive cation channel TRPM2 modulates phagocyte ROS production and inflammation JO: Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=22101731 #FOAvip 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. Twit Text FOAVip The redox-sensitive cation channel TRPM2 modulates phagocyte ROS production and inflammation ????Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=22101731 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=22101731 #FOAvip English Wikipedia <ref>{{Cite pmid|22101731}}</ref> The redox-sensitive cation channel TRPM2 modulates phagocyte ROS production and inflammation #MMPMID22101731 Di A; Gao XP; Qian F; Kawamura T; Han J; Hecquet C; Ye RD; Vogel SM; Malik AB Nat Immunol 2011[Nov]; 13 (1): 29-34 PMID22101731show ga 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. |Animals[MESH] |Calcium/metabolism[MESH] |Inflammation/genetics/*metabolism/pathology[MESH] |Lung Diseases/genetics/metabolism/pathology[MESH] |Membrane Potentials[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |Mice, Knockout[MESH] |Oxidation-Reduction[MESH] |Phagocytes/*metabolism[MESH] |Reactive Oxygen Species/*metabolism[MESH]The redox-sensitive cation channel TRPM2 modulates phagocyte ROS produ(epmc).pdf DeepDyve Pubget Overpricing