Degenerative cardiac conditions are a significant cause of morbidity and mortality following myocardial infarction. Recent evidence shows that in the area surrounding a myocardial infarcted region, there is a marked increase in the production of vascular endothelial growth factor (VEGF), a known angiogenic protein, reflecting the bodies attempt to deliver the necessary nutrients and oxygen for ongoing repair. In addition, preliminary data shows that in the areas of ischemia within the heart, there is a marked decrease in the expression of endothelial monocyte activating polypeptide (EMAP) II, a recently identified anti-angiogenic cytokine. The question we proposed to answer is whether or not EMAP II functions as an important regulator in the physiological repair process following an acute myocardial infarction. The correlation between the expression of EMAP II and VEGF will also be evaluated. The research question was investigated using a model that produced transient non-lethal myocardial ischemia in a rodent. The infarcted rodents were be sacrificed at several predetermined days post infarction. The expression and distribution EMAP II was evaluated using immunohistochemistry. Histologic results showed that an area of ischemia and revascularization following an acute infarct was achieved. We demonstrated a slight elevation of EMAP II during the early stages of revascularization, and a marked increase of the anti-angiogenic protein toward the end of revascularization. Immunohistochemistry demonstrated no EMAP II in the areas undergoing revascularization, and a decrease in the peri-infarct regions. We conclude that we have demonstrated a model of ischemia and revascularization in a rat. We also conclude that the anti-angiogenic protein EMAP II plays a role in myocardial revascularization following an acute infarct.
|Original language||English (US)|
|Journal||Journal of Investigative Medicine|
|State||Published - Feb 1999|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)