TY - JOUR
T1 - Protection against endotoxic shock as a consequence of reduced nitrosative stress in MLCK210-null mice
AU - Ranaivo, Hantamalala Ralay
AU - Carusio, Nunzia
AU - Wangensteen, Rosemary
AU - Ohlmann, Patrick
AU - Loichot, Cecile
AU - Tesse, Angela
AU - Chalupsky, Karel
AU - Lobysheva, Irina
AU - Haiech, Jacques
AU - Watterson, D. Martin
AU - Andriantsitohaina, Ramaroson
N1 - Funding Information:
Supported by Fonds de Recherche Hoechst Marion Roussel (grant GIP-HMR2): Exploration Fonctionnelle et Analyse Globale de l'Expression des Gènes, and Fondo Europeo de Desarrollo Regional no. 8891. H.R.R. was supported by the Bourse BDI of CNRS.
Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 2007/2
Y1 - 2007/2
N2 - 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-κB 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.
AB - 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-κB 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.
UR - http://www.scopus.com/inward/record.url?scp=33947508111&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33947508111&partnerID=8YFLogxK
U2 - 10.2353/ajpath.2007.060219
DO - 10.2353/ajpath.2007.060219
M3 - Article
C2 - 17255312
AN - SCOPUS:33947508111
SN - 0002-9440
VL - 170
SP - 439
EP - 446
JO - American Journal of Pathology
JF - American Journal of Pathology
IS - 2
ER -