Premium
Role of caspase‐8 in hepatocyte response to infection and injury in mice
Author(s) -
Ben Moshe Tehila,
Barash Hila,
Kang TaeBong,
Kim JinChul,
Kovalenko Andrew,
Gross Eitan,
Schuchmann Marcus,
Abramovitch Rinat,
Galun Eithan,
Wallach David
Publication year - 2007
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.21495
Subject(s) - hepatocyte , apoptosis , programmed cell death , inflammation , conditional gene knockout , liver injury , caspase , biology , cell growth , caspase 3 , immunology , microbiology and biotechnology , cancer research , gene , endocrinology , genetics , in vitro , phenotype
Caspase‐8 has been implicated in signaling for apoptotic cell death and for certain nonapoptotic functions. However, knowledge of actual physiological or pathophysiological processes to which this enzyme contributes is lacking. Using a mouse model and employing the conditional knockout approach to delete the caspase ‐ 8 gene specifically in the liver, we found that caspase‐8 deficiency in hepatocytes facilitates infection of the liver by Listeria monocytogenes , attenuates the hepatocyte proliferation wave during the first 48 hours after partial hepatectomy and, depending on the genetic background of the mice, prompts a chronic inflammatory response to the hepatectomy, as a result of which the proliferation of hepatocytes, although initially suppressed, might later be persistently enhanced, resulting in significant hepatomegaly. Conclusion: These findings indicate that caspase‐8 participates in regulation of the cellular response to infection and injury and that it does so by affecting various cellular functions, including cell death, cell proliferation, and induction of inflammation. (H EPATOLOGY 2007.)