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  • Title: Tumor necrosis factor-alpha induces c-jun during the regenerative response to liver injury.
    Author: Diehl AM, Yin M, Fleckenstein J, Yang SQ, Lin HZ, Brenner DA, Westwick J, Bagby G, Nelson S.
    Journal: Am J Physiol; 1994 Oct; 267(4 Pt 1):G552-61. PubMed ID: 7943321.
    Abstract:
    After liver injury, remaining hepatocytes proliferate to regenerate the liver. Although the precise mechanisms that initiate and localize regeneration are unknown, local induction of c-jun is a critical, early step in the response. Treatment of rats with antibodies to tumor necrosis factor-alpha (TNF-alpha), a mediator of liver injury, inhibits regenerative induction of jun nuclear kinase activity and nuclear c-jun expression and alters the DNA binding activity of the c-jun transcription factor, AP-1, in liver. Pretreatment with anti-TNF antibodies does not affect pulmonary or renal c-jun expression or AP-1 binding activity post-partial hepatectomy. In primary hepatocyte cultures, TNF-alpha directly promotes the proliferative actions of mitogens, supporting in vivo evidence that it sensitizes hepatocytes to mitogens. Thus local release of TNF may act in a paracrine fashion to initiate regeneration in the injured liver by promoting induction of critical growth-related genes, such as c-jun.
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