Research Interests
The complications of atherosclerosis such as heart attack and stroke are currently the number one and three causes of death in the US respectively. Balloon angioplasty with or without stent placement is the treatment of choice for coronary and peripheral vascular procedures. Within several months to a year one third to half of all patients develop restenosis leading to secondary procedures. Restenosis is due to the vessels response to injury combined with the body’s immune response. It is not the progression of the underlying atherosclerotic disease. The smooth muscle cells migrate from the muscular layer of the artery to the intima where they proliferate. If the smooth muscle migration could be inhibited, restenosis may be limited or possibly arrested. It is vitally important to understand the key regulators in the pathway affecting smooth muscle migration. Smooth muscle migration is also essential in the pathogenesis of atherosclerosis, transplant vasculopathy, and restenosis of bypass grafts.
The objective of our studies is to understand the role of phospholipase in smooth muscle migration during restenosis. We are performing studies looking at smooth muscle migration in cells that have been either inhibited or deficient in cytosolic phospholipase A2 (cPLA2). We hypothesize that this enzyme is a key component in the chemotaxis of smooth muscle cells. Further experiments will measure the amount of smooth muscle cells and intimal hyperplasia during restenosis in the femoral artery of mice deficient in cPLA2.
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