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CYLD deletion triggers nuclear factor-κB-signaling and increases cell death resistance in murine hepatocytes

World Journal of Gastroenterology 2014年第45期20卷 17049-17064页

作者： Toni Urbanik Bruno Christian Koehler Laura Wolpert Christin Elbner Anna-Lena Scherr Thomas Longerich Nicole Kautz Stefan Welte nadine hovelmeyer Dirk Jager Ari Waisman Henning Schulze-Bergkamen National Center for Tumor Diseases Department of Medical Oncology University Clinic of Heidelberg 69120 HeidellbergBade-WuerrtembergGermany Institute of Pathology University Hospital Heidelberg 69120 HeidelbergBaden-WuerrtembergGermany Institute for Molecular Medicine Johannes Gutenberg-University Mainz 55131 MainzRheinland-PalatlnateGemany

AIM:To analyze the role of CYLD for receptor-mediated cell death of murine hepatocytes in acute liver injury ***:Hepatocyte cell death in CYLD knockout mice(CYLD-/-)was analyzed by application of liver injury models for CD95-(Jo2)and tumor necrosis factor(TNF)-α-[D-Gal N/lipopolysaccharide(LPS)]induced *** injury was assessed by measurement of serum transaminases and histological *** induction was quantified by cleaved PARP staining and Western blotting of activated *** factor(NF)-κB,ERK,Akt and jun amino-terminal kinases signaling were *** Hepatocytes were isolated by two step-collagenase perfusion and treated with recombinant TNF-αand with the CD95-ligand *** viability was analyzed by ***:Livers of CYLD-/-mice showed increased anti-apoptotic NF-κB *** both applied liver injury models CYLD-/-mice showed a significantly reduced apoptosis *** D-Gal N/LPS treatment CYLD-/-mice exhibited significantly lower levels of alanine aminotransferase(ALT)(295 U/L vs 859 U/L,P<0.05)and aspartate aminotransferase(AST)(560 U/L vs 1025 U/L,P<0.01).After Jo injection CYLD-/-mice showed 2-fold lower ALT(50 U/L vs 110 U/L,P<0.01)and lower AST(250 U/L vs 435 U/L,P<0.01)serumlevels compared to WT *** addition,isolated CYLD-/-primary murine hepatocytes(PMH)were less sensitive towards death receptor-mediated apoptosis and showed increased levels of Bcl-2,XIAP,c IAP1/2,survivin and c-FLIP expression upon TNF-and CD95-receptor triggering,*** of NF-κB activation by the inhibitor of NF-κB phosphorylation inhibitor BAY 11-7085 inhibited the expression of antiapoptotic proteins and re-sensitized CYLD-/-PMH towards TNF-and CD95-receptor mediated cell ***:CYLD is a central regulator of apoptotic cell death in murine hepatocytes by controlling NF-κB dependent anti-apoptotic signaling.

关键词： CYLD Apoptosis Nuclear factor-κB Tumo rnecrosis factor-α CD95 Liver

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