| First Author | Kühnle S | Year | 1999 |
| Journal | Biochem Biophys Res Commun | Volume | 263 |
| Issue | 2 | Pages | 433-8 |
| PubMed ID | 10491311 | Mgi Jnum | J:57849 |
| Mgi Id | MGI:1345877 | Doi | 10.1006/bbrc.1999.1393 |
| Citation | Kuhnle S, et al. (1999) Prevention of endotoxin-induced lethality, but not of liver apoptosis in poly(ADP-ribose) polymerase-deficient mice. Biochem Biophys Res Commun 263(2):433-8 |
| abstractText | Activation of poly-(ADP-ribose) polymerase (PARP) is often associated with cytotoxicity, but its precise role in shock-induced lethality and in different modes of tissue injury is still unknown. We took advantage of the existence of mice with a targeted deletion of the PARP gene (PARP-/-) to examine the differential sensitivity of wild-type (wt) and PARP-/- mice toward endotoxin (LPS)-induced lethality and different forms of liver damage. All PARP-/- animals survived high-dose (20 mg/kg) LPS-mediated shock, which killed 60% of wt animals. Moreover, LPS-induced necrotic liver damage was significantly reduced. In contrast, when apoptotic liver damage was induced via injection of low concentrations of LPS (30 microgram/kg) into D-galactosamine-sensitized mice, or via activation of hepatic cell death receptors, PARP-/- animals were not protected. We conclude that PARP is involved in systemic LPS toxicity, while it plays a minor role in apoptotic liver damage mediated by TNF or CD95. Copyright 1999 Academic Press. |
