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Published on: April 9, 2018
Leukocyte and endothelial adhesion molecule studies in knockout mice
1Department of Medicine, Division of Cardiology, Louisiana State University Health Sciences Center, 1501 Kings Highway, Shreveport, LA 71130, USA.
Insights
Leukocyte adhesion molecules like CD18 and intercellular adhesion molecule-1 mediate heart injury after ischemia and reperfusion. Targeting these molecules reduces myocardial damage, offering therapeutic potential.
Area of Science:
- Cardiovascular Biology
- Immunology
- Inflammation Research
Background:
- Myocardial ischemia and reperfusion (I/R) triggers an inflammatory response, with leukocytes contributing significantly to injury.
- Leukocyte-endothelial cell adhesion molecules mediate neutrophil interactions in coronary vasculature post-I/R.
Purpose of the Study:
- To investigate the role of specific adhesion molecules in mediating myocardial I/R injury.
- To assess the therapeutic potential of targeting leukocyte-endothelial interactions.
Main Methods:
- Studies involved genetic deficiency models (CD18, intercellular adhesion molecule-1, P-selectin, E-selectin deficient mice).
- Evaluation of myocardial necrosis and neutrophil accumulation following I/R injury.
Main Results:
- Genetic deficiency of CD18 significantly attenuated myocardial I/R injury.
- Absence of intercellular adhesion molecule-1 minimized myocardial necrosis.
- P-selectin and E-selectin deficiency studies showed reduced neutrophil accumulation and myocardial injury.
Conclusions:
- Leukocyte adhesion molecules, including beta(2)-integrins (CD18) and intercellular adhesion molecule-1, are critical in mediating myocardial I/R injury.
- Selectins also play a role in leukocyte-endothelial interactions during I/R.
- Targeting these adhesion pathways presents a potential therapeutic strategy for reducing I/R-induced heart damage.
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.
