Immuno-Regulatory Control of Atherosclerosis via Apolipoprotein E
A longstanding interest of the lab is to study mechanisms through which a protein called apolipoprotein E (ApoE) contributes to suppress the progression of atherosclerosis and promote its regression in an isoform-specific manner. To this end, we study mouse models of conditional apoE expression developed in our laboratory that we have termed HypoE mice.
Our recent studies revealed that apoE has a capacity to suppress atherosclerosis beyond its recognized ability to reduce plasma lipid levels. Cellular apoE expression in myeloid cells was found to modulate microRNA biogenesis, resulting in increased levels of microRNA-146a thereby enhancing a natural negative feedback mechanism to suppress NF-kB driven inflammation and atherosclerosis.
Diabetic Hyperglycemia in Symptomatic Forms Of CAD And PAD
Hyperglycemia, or high blood sugar (glucose), is a serious health problem for those with diabetes. Hyperglycemia develops when there is too much sugar in the blood. We are investigating the role of diabetic hyperglycemia in enhancing symptomatic forms of CAD and PAD, and the influence on the regression of atherosclerosis and outcome of heart failure after myocardial infarction.