Elevated postischemic tissue injury and leukocyte-endothelial adhesive interactions in mice with global deficiency in caveolin-2: role of PAI-1

Author:

Liu Yajun1,Wang Meifang1,Wang Derek1,Fay William P.12,Korthuis Ronald J.13,Sowa Grzegorz1

Affiliation:

1. Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, Missouri

2. Department of Medicine, University of Missouri, Columbia, Missouri

3. The Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri

Abstract

The role of caveolin-2 in regulating ischemia/reperfusion (I/R) tissue injury and the mechanisms underlying its effects are unknown. This study uses caveolin-2-deficient mouse and small intestinal I/R injury models to examine the role of caveolin-2 in the leukocyte-dependent reperfusion injury. We demonstrate for the first time that caveolin-2 plays a protective role from the I/R-induced leukocyte-dependent reperfusion injury by reducing PAI-1 protein levels in intestinal tissue and leukocyte-endothelial adhesive interactions in postcapillary venules.

Funder

HHS | NIH | National Heart, Lung, and Blood Institute

HHS | NIH | National Institute on Alcohol Abuse and Alcoholism

U.S. Department of Defense

Publisher

American Physiological Society

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology

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