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Activation of the 55 kDa TNF receptor is necessary and sufficient for TNF-induced liver failure, hepatocyte apoptosis, and nitrite release

Activation of the 55 kDa TNF receptor is necessary and sufficient for TNF-induced liver failure, hepatocyte apoptosis, and nitrite release

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Prüfsumme: MD5:4f7369857748c25a4b9d8ebc78264e6f

LEIST, Marcel, Florian GANTNER, Sabine JILG, Albrecht WENDEL, 1995. Activation of the 55 kDa TNF receptor is necessary and sufficient for TNF-induced liver failure, hepatocyte apoptosis, and nitrite release. In: Journal of Immunology(154), pp. 1307-1316

@article{Leist1995Activ-7447, title={Activation of the 55 kDa TNF receptor is necessary and sufficient for TNF-induced liver failure, hepatocyte apoptosis, and nitrite release}, year={1995}, number={154}, journal={Journal of Immunology}, pages={1307--1316}, author={Leist, Marcel and Gantner, Florian and Jilg, Sabine and Wendel, Albrecht} }

The systemic inflammatory response is characterized by release of circulating TNF which may cause multiorgan failure including septic liver failure. We studied TNF signaling in an appropriate in vitro system with primary murine hepatocyte cultures from normal and genetically altered animals. Either one of the three different TNF species, huTNF-alpha, huTNF-beta, or muTNF-alpha (at concentrations > 1 ng/ml) induced direct hepatocytotoxicity preceded by DNA fragmentation in cells prepared from wild-type C57BL mice. TNF-induced cytotoxicity was preceded by oligonucleosomal DNA fragmentation. Further cellular responses to TNF exposure were induction of nitric oxide synthase and secretion of serum amyloid A. None of the above events occurred in hepatocytes lacking the gene for the 55-kDa TNF receptor (TNF-R1), even after stimulation with > 1 μ/ml TNF. However, selective stimulation of the TNF-R1 in wild-type hepatocytes with huTNF-alpha elicited a pattern of responses essentially similar to that seen with muTNF-alpha. We obtained analogous results when we examined the hepatotoxicity of TNF in D-galactosamine-sensitized mice, i.e., DNA fragmentation and liver failure was noted in wild-type mice, whereas TNF-R1-deficient mice were completely resistant. We conclude that the TNF-R1 is not only necessary, but also sufficient for TNF signaling in murine hepatocytes. Leist, Marcel 2011-03-24T17:34:30Z application/pdf Activation of the 55 kDa TNF receptor is necessary and sufficient for TNF-induced liver failure, hepatocyte apoptosis, and nitrite release Jilg, Sabine Wendel, Albrecht Leist, Marcel Jilg, Sabine 2011-03-24T17:34:30Z Gantner, Florian First publ. in: Journal of Immunology (1995), 154, 3, pp. 1307-1316 1995 Gantner, Florian eng Wendel, Albrecht deposit-license

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