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Dadun > Depósito Académico > CIMA (Centro de Investigación Médica Aplicada) > Área de Terapia génica y Hepatología > Anticuerpos monoclonales > DA - CIMA - Terapia génica y Hepatología - Anticuerpos monoclonales - Artículos de Revista >

Cardiotrophin-1 defends the liver against ischemia-reperfusion injury and mediates the protective effect of ischemic preconditioning
Authors: Iñiguez, M. (María)
Berasain, C. (Carmen)
Martinez-Anso, E. (Eduardo)
Bustos, M. (Matilde)
Fortes, P. (Puri)
Pennica, D. (Dianne)
Avila, M.A. (Matías Antonio)
Prieto, J. (Jesús)
Keywords: Cytokines/physiology
Ischemic Preconditioning
Reperfusion Injury/metabolism
Issue Date: 2006
Publisher: Rockefeller University Press
Publisher version: http://dx.doi.org/10.1084/jem.20061421
ISSN: 0022-1007
Citation: Iñiguez M, Berasain C, Martinez-Anso E, Bustos M, Fortes P, Pennica D, et al. Cardiotrophin-1 defends the liver against ischemia-reperfusion injury and mediates the protective effect of ischemic preconditioning. J Exp Med 2006 Dec 25;203(13):2809-2815.
Abstract
Ischemia-reperfusion (I/R) liver injury occurs when blood flow is restored after prolonged ischemia. A short interruption of blood flow (ischemic preconditioning [IP]) induces tolerance to subsequent prolonged ischemia through ill-defined mechanisms. Cardiotrophin (CT)-1, a cytokine of the interleukin-6 family, exerts hepatoprotective effects and activates key survival pathways like JAK/STAT3. Here we show that administration of CT-1 to rats or mice protects against I/R liver injury and that CT-1-deficient mice are exceedingly sensitive to this type of damage. IP markedly reduced transaminase levels and abrogated caspase-3 and c-Jun-NH2-terminal kinase activation after I/R in normal mice but not in CT-1-null mice. Moreover, the protective effect afforded by IP was reduced by previous administration of neutralizing anti-CT-1 antibody. Prominent STAT3 phosphorylation in liver tissue was observed after IP plus I/R in normal mice but not in CT-1-null mice. Oxidative stress, a process involved in IP-induced hepatoprotection, was found to stimulate CT-1 release from isolated hepatocytes. Interestingly, brief ischemia followed by short reperfusion caused mild serum transaminase elevation and strong STAT3 activation in normal and IL-6-deficient mice, but failed to activate STAT3 and provoked marked hypertransaminasemia in CT-1-null animals. In conclusion, CT-1 is an essential endogenous defense of the liver against I/R and is a key mediator of the protective effect induced by IP.
Permanent link: http://hdl.handle.net/10171/20306
Appears in Collections:DA - CIMA - Terapia génica y Hepatología - Vectores - Artículos de revista
DA - CIMA - Terapia génica y Hepatología - Oncobiología - Artículos de revista
DA - CIMA - Terapia génica y Hepatología - Hepatología bioquímica - Artículos de revista
DA - CIMA - Terapia génica y Hepatología - Anticuerpos monoclonales - Artículos de Revista

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