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The composition of vulnerable atherosclerotic plaques has been defined in humans.  A paradigm shift has occurred that emphasizes the composition of vulnerable plaques rather than the magnitude of obstruction as the pivotal determinant of acute coronary syndromes.  A particular strength of our program is the development of an imaging technique that quantifies the composition of vascular lesions in transgenic mice and other organisms with atherosclerosis.  The apolipoprotein E deficient mouse develops a neointima that exhibits substantial smooth muscle cell content.

Efforts are underway to alter migration, proliferation, and apoptosis of vascular smooth muscle cells in order to generate transgenic mice that exhibit a hypocellular neointima that is expected to be more prone to rupture.  The progression of atherosclerosis in mice that manifest diabetes and insulin resistance is under active investigation as well.  Phenotypic alteration of vascular smooth muscle cells is a seminal feature of atherosclerotic lesions.  Efforts to define intracellular signaling mechanisms responsible for this phenotypic change entail characterization of interaction, between single stranded DNA and transcription factors.

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