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Ron receptor-dependent gene regulation in a mouse model of endotoxin-induced acute liver failure

Hepatobiliary & Pancreatic Diseases International 2012年第4期11卷 383-392页

作者： Rishikesh M Kulkarni louis w kutcher william D Stuart Daniel J Carson Mike A Leonis Susan E waltz Departments of Cancer and Cell Biology University of CincinnatiCincinnatiOH 45267-0521USA Biology University of CincinnatiCincinnatiOH 45267-0521USA Division of Gastroenterology Hepatology and NutritionCincinnati Children's Hospital Medical CenterCincinnatiOH 45229USA Department of Research Shriner's Hospital for Children and Cincinnati Veterans Affairs Medical CenterCincinnatiOH 45267-0521USA

BACKGROUND:Prior experimentation has shown that loss of the tyrosine kinase(TK) signaling domain of the Ron receptor leads to marked hepatocyte protection in a model of lipopolysaccharideinduced acute liver failure(ALF) in D-galactosamine(GalN)sensitized *** aim of this study was to identify the role of Ron in the regulation of hepatic gene ***:Microarray analyses were performed on liver RNA isolated sequentially from wild-type(wT) and TK-/mice during the progression of *** array data were validated using western and immunohistochemistry analyses as well as with ex vivo culture ***:At baseline,101 genes were differentially expressed between wT and TK-/-livers,which regulate processes involved in hypoxia,proliferation,apoptosis and *** hour after ALF induction,wT livers exhibited increased cytokine expression compared to TK-/-livers,and after 4 hours,an induction of suppressor of cytokine signaling(SOCS) genes as well as JAK-STAT pathway activation were prominent in TK-/livers compared to ***:Our studies suggest a novel hepato-protective mechanism in Ron TK-/-mice wherein increased and sustained SOCS production and JAK-STAT activation in the hepatocyte may inhibit the destructive proinflammatory milieu and promote survival factors which blunt hepatic death and the ensuing development of ALF.

关键词： Mst1R suppressors of cytokine signaling Met receptor hepatocyte growth factor-like protein

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