作者: Torsten Wuestefeld , Christian Klein , Konrad L. Streetz , Ulrich Betz , Jörg Lauber
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摘要: After tissue loss the liver has unique capacity to restore its mass by hepatocyte proliferation. Interleukin-6 (IL6)-deficient mice show a lack in DNA synthesis after partial hepatectomy (PH). To define better role of IL6 and family members for regeneration PH, we used conditional knockout glycoprotein 130 (gp130), common signal transducer all members. We that gp130-dependent pathways control Stat3 activation PH. By using gene array analysis, demonstrate c-jun, NF-κB, c-myc, tumor necrosis factor receptor expression is gp130-dependent. However, gp130-deleted only minor effects on cell cycle maximum PH were found compared with controls. As gp130 animals, acute phase response was completely abolished, considered other means are essential regeneration. LPS stimulation also −/− animals leads significant reduction survival synthesis, which associated decreased Bcl-xL higher apoptosis liver. These results indicate phenotype concerning might be linked degree infection Thus our suggest signaling not direct influence progression but activate protective important enable