Format

Send to

Choose Destination
Curr Opin Pharmacol. 2004 Apr;4(2):154-8.

Leukocyte and endothelial adhesion molecule studies in knockout mice.

Author information

1
Department of Medicine, Division of Cardiology, Louisiana State University Health Sciences Center, 1501 Kings Highway, Shreveport, LA 71130, USA.

Abstract

Ischemia and reperfusion of the myocardium initiate an inflammatory response directed against the myocardium, and many studies attribute a significant portion of this injury to leukocytes. Leukocyte and endothelial cell adhesion molecules are responsible for neutrophil-endothelial cell interactions in coronary vasculature following ischemia and reperfusion. Interactions between beta(2)-integrins and intercellular adhesion molecule-1 are responsible for firm adhesion of neutrophils to the coronary endothelium in acute cardiac inflammation. Leukocyte-expressed CD18 plays a crucial role, and genetic deficiency of CD18 significantly attenuates myocardial ischemia-reperfusion injury. Genetic deficiency of intercellular adhesion molecule-1 also minimizes myocardial necrosis following ischemia and reperfusion. The selectin family of adhesion glycoproteins also participates in various phases of leukocyte-endothelial interactions, and studies with P-selectin- and E-selectin-deficient mice have shown attenuation of both neutrophil accumulation and myocardial injury following myocardial ischemia and reperfusion.

PMID:
15063359
DOI:
10.1016/j.coph.2004.01.003
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center