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Office: 803 253 5842
Fax: 803 733 3192
E-mail: carnevale
gw.med.sc.edu
Department of Pathology, Microbiology
and Immunology,
University
of South Carolina School of Medicine, Columbia, SC 29208 |
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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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