The plasminogen activator inhibitor-2 gene is not required for normal murine development or survival

Kristiann M. Dougherty, Julia M. Pearson, Angela Y. Yang, Randal J. Westrick, Mark S. Baker, David Ginsburg*

*Corresponding author for this work

Research output: Contribution to journalArticle

93 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)686-691
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume96
Issue number2
DOIs
Publication statusPublished - 19 Jan 1999
Externally publishedYes

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