Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2004-4-5
pubmed:abstractText
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1471-4892
pubmed:author
pubmed:issnType
Print
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
154-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Leukocyte and endothelial adhesion molecule studies in knockout mice.
pubmed:affiliation
Department of Medicine, Division of Cardiology, Louisiana State University Health Sciences Center, 1501 Kings Highway, Shreveport, LA 71130, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review