Research Focus and Highlights
We are interested in how innate immunity contributes to early inflammatory events in atherosclerosis. Smooth muscle cells constitute the primary cell type in healthy arteries, and in their normal differentiated, contractile state they regulate vascular tone and blood pressure. These cells also have remarkable phenotypic plasticity, and under dramatic phenotypic changes, as a prelude to the disease process, including increased proliferation and synthesis of pro-inflammatory cytokines and chemokines, and extracellular matrix proteins. Although these events begin in early childhood and precede lesion development by several decades, they set the stage for later devastating diseases such as coronary artery disease and stroke. Our current research is using transgenic mouse models to determine how Toll-like receptors 2 and 4 contribute to phenotypic switching in smooth muscle cells, and to arterial inflammation and the accumulation of intimal lipid in the setting of hypercholesterolemia. We are particularly interested in how SMC may regulate monocyte or T cell recruitment to lesions.
Research Administrator: Dionne Bradford