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Título: | Growth arrest-specific protein 6 is hepatoprotective against murine ischemia/reperfusion injury |
Autor: | Llacuna Duran, Laura CSIC; Bárcena, Cristina CSIC ORCID; Bellido-Martín, Lola CSIC; Fernández Fernández, Laura CSIC; Stefanovic, Milica CSIC; Marí, Montserrat CSIC ORCID ; García-Ruiz, Carmen CSIC ORCID ; Fernández-Checa, José C. CSIC ORCID; García de Frutos, Pablo CSIC ORCID ; Morales, Albert CSIC ORCID | Fecha de publicación: | 2010 | Editor: | Wiley-Blackwell | Citación: | Hepatology 52(4): 1371-1379 (2010) | Resumen: | Growth arrest specific gene 6 (GAS6) promotes growth and cell survival during tissue repair and development in different organs, including the liver. However, the specific role of GAS6 in liver ischemia/reperfusion (I/R) injury has not been previously addressed. Here we report an early increase in serum GAS6 levels after I/R exposure. Moreover, unlike wild-type (WT) mice, Gas(-/-) mice were highly sensitive to partial hepatic I/R, with 90% of the mice dying within 12 hour; of reperfusion because of massive hepatocellular injury. I/R induced early hepatic protein kinase B (AICT) phosphorylation in WT mice but not in GasC mice without significant changes in c-Jun N-terminal kinase phosphorylation or nuclear factor kappa B translocation, whereas hepatic interleukin-1 beta (IL-1 beta) and tumor necrosis Factor (TNF) messenger RNA levels were higher in Gas6(-/-). mice versus WT mice. In line with the in vivo data, in vitro studies indicated that GAS6 induced AKT phosphorylation in primary mouse hepatocytes and thus protected them from hypoxia-induced cell death, whereas GAS6 diminished fipopolysaccharideinduced cytokine expression (IL-1 beta and TNF) in murine macrophages. Finally, recombinant GAS6 treatment in vivo not only rescued GAS6 knockout mice from severe I/R-induced liver damage but also attenuated hepatic damage in WT mice after I/R. Conclusion: Our data have revealed GAS6 to be a new player in liver I/R injury that is emerging as a potential therapeutic target for reducing postischemic hepatic damage. | Descripción: | El pdf del artículo es el manuscrito de autor: PMCID:PMC2947564 | Versión del editor: | http://dx.doi.org/10.1002/hep.23833 | URI: | http://hdl.handle.net/10261/77741 | DOI: | 10.1002/hep.23833 | Identificadores: | issn: 0270-9139 e-issn: 1527-3350 |
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