| First Author | van Molle W | Year | 1999 |
| Journal | FEBS Lett | Volume | 445 |
| Issue | 1 | Pages | 115-8 |
| PubMed ID | 10069384 | Mgi Jnum | J:53244 |
| Mgi Id | MGI:1331559 | Doi | 10.1016/s0014-5793(99)00109-x |
| Citation | van Molle W, et al. (1999) Caspase-1 is not involved in experimental hepatitis in mouse. FEBS Lett 445(1):115-8 |
| abstractText | Experimental hepatitis induced by tumor necrosis factor in D-(+)-galactosamine-sensitized mice or by an agonistic anti-Fas antibody in normal mice is accompanied by dramatic apoptosis of hepatocytes. Apoptosis is the final result of activation of a cascade of caspases. We used caspase-1-/- mice, generated by gene targeting, to study the role of this protease in TNF- and anti-Fas-induced lethal hepatitis. We found that mutant mice exhibited the typical caspase-1-/- phenotype, since they resisted to a lethal injection of LPS and released no interleukin-1beta in the circulation, in contrast to wild-type littermates. When caspase-1-/- mice were challenged with different doses of tumor necrosis factor/D-(+)-galactosamine or with anti-Fas, no increased survival was observed compared with control mice. Furthermore, apoptosis in the livers of these mice and serum levels of alanine aminotransferase were not reduced. These data indicate that caspase-1 deficiency does not lead to reduced apoptosis in these models, either because caspase-1 is irrelevant in this model or because of functional redundancy. |
