Effects of sodium nitroprusside on hemodialysis-induced platelet activation |
| |
Authors: | B Jilma N Hergovich P Stohlawetz G Stummvoll S Albinni S Simak S Schmaldienst E Pohanka HG Eichler S Kapiotis |
| |
Affiliation: | Howard Hughes Medical Institute, University of Michigan Medical School, Ann Arbor, MI 48109-0650, USA. |
| |
Abstract: | Plasminogen activator inhibitor-2 (PAI-2), a member of the serpin gene family, is thought to serve as a primary regulator of plasminogen activation in the extravascular compartment. High levels of PAI-2 are found in keratinocytes, monocytes, and the human trophoblast, the latter suggesting a role in placental maintenance or embryo development. The primarily intracellular distribution of PAI-2 also may indicate a unique regulatory role in a protease-dependent cellular process such as apoptosis. To examine the potential functions of PAI-2 in vivo, we generated PAI-2-deficient mice by gene targeting in embryonic stem cells. Homozygous PAI-2-deficient mice exhibited normal development, survival, and fertility and were also indistinguishable from normal controls in response to a bacterial infectious challenge or endotoxin infusion. No differences in monocyte recruitment into the peritoneum were observed after thioglycollate injection. Epidermal wound healing was equivalent among PAI-2 -/- null and control mice. Finally, crossing PAI-2 -/- with PAI-1 -/- mice to generate animals deficient in both plasminogen activator inhibitors failed to uncover an overlap in function between these two related proteins. |
| |
Keywords: | |
本文献已被 PubMed 等数据库收录! |
|