PuSH - Publikationsserver des Helmholtz Zentrums München: RIP3 inhibits inflammatory hepatocarcinogenesis but promotes cholestasis by controlling caspase-8- and JNK-dependent compensatory cell proliferation.

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Vucur, M.* ; Reisinger, F. ; Gautheron, J.* ; Janssen, J.* ; Roderburg, C.* ; Cardenas, D.V.* ; Kreggenwinkel, K.* ; Koppe, C.* ; Hammerich, L.* ; Hakem, R.* ; Unger, K. ; Weber, A.* ; Gassler, N.* ; Luedde, M.* ; Frey, N.* ; Neumann, U.P.* ; Tacke, F.* ; Trautwein, C.* ; Heikenwälder, M. ; Luedde, T.*

RIP3 inhibits inflammatory hepatocarcinogenesis but promotes cholestasis by controlling caspase-8- and JNK-dependent compensatory cell proliferation.

Cell Rep. 4, 776-790 (2013)

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For years, the term "apoptosis" was used synonymously with programmed cell death. However, it was recently discovered that receptor interacting protein 3 (RIP3)-dependent "necroptosis" represents an alternative programmed cell death pathway activated in many inflamed tissues. Here, we show in a genetic model of chronic hepatic inflammation that activation of RIP3 limits immune responses and compensatory proliferation of liver parenchymal cells (LPC) by inhibiting Caspase-8-dependent activation of Jun-(N)-terminal kinase in LPC and nonparenchymal liver cells. In this way, RIP3 inhibits intrahepatic tumor growth and impedes the Caspase-8-dependent establishment of specific chromosomal aberrations that mediate resistance to tumor-necrosis-factor-induced apoptosis and underlie hepatocarcinogenesis. Moreover, RIP3 promotes the development of jaundice and cholestasis, because its activation suppresses compensatory proliferation of cholangiocytes and hepatic stem cells. These findings demonstrate a function of RIP3 in regulating carcinogenesis and cholestasis. Controlling RIP3 or Caspase-8 might represent a chemopreventive or therapeutic strategy against hepatocellular carcinoma and biliary disease.

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