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(American Journal of Pathology. 2007;170:439-446.)
© 2007 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2007.060219

Protection Against Endotoxic Shock as a Consequence of Reduced Nitrosative Stress in MLCK210-Null Mice

Hantamalala Ralay Ranaivo*{dagger}, Nunzia Carusio*{ddagger}, Rosemary Wangensteen*, Patrick Ohlmann*, Cecile Loichot*, Angela Tesse*{ddagger}, Karel Chalupsky*, Irina Lobysheva§, Jacques Haiech{dagger}, D. Martin Watterson* and Ramaroson Andriantsitohaina*{ddagger}

From Unité Mixte de Recherche (UMR) Centre National de la Recherche Scientifique (CNRS) 7034,* Faculté de Pharmacie, Illkirch, France; the Center for Drug Discovery and Chemical Biology,{dagger} Northwestern University, Chicago, Illinois; UMR INSERM 771–CNRS 6214,{ddagger} Faculté de Médecine, Angers, France; and Institute of Chemical Physics RAS,§ Moscow, Russia

This study investigated the consequences of deletion of the long isoform of myosin light chain kinase (MLCK210) on the cardiovascular changes induced by the bacterial endotoxin lipopolysaccharide (LPS) and cecal ligation puncture using MLCK210–/– mice. Here, we provide evidence that deletion of MLCK210 enhanced survival after intraperitoneal injection of LPS or cecal ligation puncture. LPS-induced vascular hyporeactivity to vasoconstrictor agents was completely prevented in aorta from MLCK210–/– mice. This was associated with a decreased up-regulation of nuclear facor-{kappa}B expression and activity, inducible nitric-oxide synthase, and level of oxidative stress in the vascular media. Furthermore, LPS-induced increase of nitric oxide production in the circulation and tissues (including heart, liver, and lung) that was correlated with an increased expression of inducible nitric-oxide synthase was also reduced in MLCK210–/– mice. These data demonstrate a role for MLCK210 in endotoxin shock injury associated with oxidative and nitrosative stresses and vascular hyporeactivity.




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