PMID: 12763364May 24, 2003Paper

Sensitization by interleukin-6 of rat hepatocytes to tumor necrosis factor alpha-induced apoptosis

Journal of Hepatology
Ulrike BöerGerhard P Püschel

Abstract

Tumor necrosis factor (TNF) elicits hepatocyte apoptosis in toxic liver injury and is also central in hepatocyte proliferation after partial hepatectomy. In both circumstances interleukin (IL)-6 levels are also elevated. In mouse liver IL-6 attenuated Fas receptor-mediated apoptosis indicating its interference with pro-apoptotic signal chains. It was, therefore, the aim to examine the modulation by IL-6 of TNFalpha-induced apoptosis in rat hepatocytes. Primary rat hepatocytes were treated with IL-6 prior to induction of apoptosis with TNFalpha/actinomycin D or anti-Fas antibody M-20. Apoptosis was detected by determination of caspase-3 activation and bisbenzimide staining of condensed nuclei. Expression of TNFalpha receptors was analyzed by semi-quantitative polymerase chain reaction and ligand binding studies with [125I]-TNFalpha. IL-6 treatment doubled TNFalpha/actinomycin D-induced caspase-3 activity and significantly enhanced chromatin condensation. By contrast IL-6 inhibited Fas-induced increase in caspase-3 activity by 45% and significantly reduced chromatin condensation. IL-6 increased the mRNA level of TNF-R1 1.35-fold and augmented cell surface binding of [125I]-TNFalpha 3-fold. The latter and TNFalpha-mediated caspase...Continue Reading

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Citations

Sep 10, 2013·Archives of Toxicology·Mathieu VinkenVera Rogiers

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