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Expression of E-selectin on coronary endothelium after myocardial ischemia and reperfusion
1Division of Cardiothoracic Surgery, University of Washington, Seattle.
Insights
Neutrophils are recruited to damaged heart muscle via E-selectin, a molecule upregulated on blood vessel cells after ischemia and reperfusion. This finding sheds light on myocardial reperfusion injury mechanisms.
Area of Science:
- Cardiovascular Biology
- Immunology
- Pathology
Background:
- Neutrophils contribute to myocardial reperfusion injury and stunning.
- Understanding neutrophil recruitment mechanisms in ischemic myocardium is crucial.
Purpose of the Study:
- To investigate the role of E-selectin in neutrophil recruitment to ischemic myocardium.
- To examine the expression of E-selectin on coronary endothelium following ischemia and reperfusion.
Main Methods:
- Adult rhesus monkeys underwent coronary artery ligation followed by reperfusion.
- Immunohistochemical staining was used to analyze E-selectin expression in myocardial tissues.
Main Results:
- E-selectin was not constitutively expressed on coronary endothelium in vivo.
- E-selectin was upregulated on endothelial cells in postcapillary coronary venules post-ischemia/reperfusion.
Conclusions:
- E-selectin upregulation suggests a role in neutrophil recruitment to ischemic myocardium.
- This mechanism may be similar to neutrophil recruitment in other inflamed tissues.
Abstract:
Neutrophils localize in ischemic or infarcted myocardium and thus are implicated in playing a role in myocardial reperfusion injury and stunning. We studied one of the mechanisms by which neutrophils are recruited into the region of ischemic myocardium. Anesthetized adult rhesus monkeys (n = 2) underwent ligation of one of the obtuse marginal coronary arteries for 90 minutes followed by 5 hours of reperfusion. Tissues from the normal perfused area of the heart and from the ischemic area were preserved in methacarn fixative after sacrificing the animal at the end of the reperfusion period. Immunohistochemical staining showed that E-selectin is not constitutively expressed on coronary endothelium in vivo. E-selectin, however, was upregulated in selective endothelial cells located in the postcapillary coronary venules in response to ischemia and reperfusion. The presence of E-selectin in this setting suggests that it may have a similar role as in the recruitment of neutrophils into other inflamed or damaged tissues.