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8 results on '"Carusio, Nunzia"'

4. Protection against endotoxic shock as a consequence of reduced nitrosative stress in MLCK210-null mice

Author

UCL - MD/MINT - Département de médecine interne, Ralay Ranaivo, Hantamalala, Carusio, Nunzia, Wangensteen, Rosemary, Ohlmann, Patrick, Loichot, Cecile, Tesse, Angela, Chalupsky, Karel, Lobysheva, Irina, Haiech, Jacques, Watterson, Martin D., Andriantsitohaina, Ramaroson, UCL - MD/MINT - Département de médecine interne, Ralay Ranaivo, Hantamalala, Carusio, Nunzia, Wangensteen, Rosemary, Ohlmann, Patrick, Loichot, Cecile, Tesse, Angela, Chalupsky, Karel, Lobysheva, Irina, Haiech, Jacques, Watterson, Martin D., and Andriantsitohaina, Ramaroson

Abstract

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-kappaB 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.

Published
2007

8. Altered contractile response due to increased beta3-adrenoceptor stimulation in diabetic cardiomyopathy: the role of nitric oxide synthase 1-derived nitric oxide.

Author

Amour J, Loyer X, Le Guen M, Mabrouk N, David JS, Camors E, Carusio N, Vivien B, Andriantsitohaina R, Heymes C, and Riou B

Subjects
Animals, Blotting, Western methods, Cardiomyopathies metabolism, Diabetes Complications physiopathology, Disease Models, Animal, Echocardiography methods, Electron Spin Resonance Spectroscopy methods, Male, Myocardium enzymology, Myocytes, Cardiac metabolism, Organ Culture Techniques, Rats, Rats, Wistar, Adrenergic beta-Agonists pharmacology, Cardiomyopathies physiopathology, Diabetes Complications metabolism, Myocardial Contraction drug effects, Nitric Oxide metabolism, Nitric Oxide Synthase metabolism, Receptors, Adrenergic, beta drug effects
Abstract

Background: In the diabetic heart, the positive inotropic response to beta-adrenoceptor stimulation is altered and beta1 and beta2 adrenoceptors are down-regulated, whereas beta3 adrenoceptor is up-regulated. In heart failure, beta3-adrenoceptor stimulation induces a negative inotropic effect that results from endothelial nitric oxide synthase (NOS3)-derived nitric oxide production. The objective of our study was to investigate the role of beta3-adrenoceptor in diabetic cardiomyopathy., Methods: beta-Adrenergic responses were investigated in vivo (dobutamine echocardiography) and in vitro (left ventricular papillary muscle) in healthy and streptozotocin-induced diabetic rats. The effect of beta3-adrenoceptor inhibition on the inotropic response was studied in vitro. Immunoblots and NOS activities were performed in heart homogenates (electron paramagnetic resonance) and isolated cardiomyocytes. Data are mean percentage of baseline +/- SD., Results: The impaired positive inotropic effect was confirmed in diabetes both in vivo (121 +/- 15% vs. 160 +/- 16%; P < 0.05) and in vitro (112 +/- 5% vs. 179 +/- 15%; P < 0.05). In healthy rat, the positive inotropic effect was not significantly modified in presence of beta3-adrenoceptor antagonist (174 +/- 20%), nonselective NOS inhibitor (N -nitro-l-arginine methylester [l-NAME]; 183 +/- 19%), or selective NOS1 inhibitor (vinyl-l-N-5-(1-imino-3-butenyl)-l-ornithine [l-VNIO]; 172 +/- 13%). In diabetes, in parallel with the increase in beta3-adrenoceptor protein expression, the positive inotropic effect was partially restored by beta3-adrenoceptor antagonist (137 +/- 8%; P < 0.05), l-NAME (133 +/- 11%; P < 0.05), or l-VNIO (130 +/- 13%; P < 0.05). Nitric oxide was exclusively produced by NOS1 within diabetic cardiomyocytes. NOS2 and NOS3 proteins were undetectable., Conclusions: beta3-Adrenoceptor is involved in altered positive inotropic response to beta-adrenoceptor stimulation in diabetic cardiomyopathy. This effect is mediated by NOS1-derived nitric oxide in diabetic cardiomyocyte.

Published
2007
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