Role for the Rho-GAP Graf3 in the Pathogenesis of Human Hypertension

My research interests include defining the signaling networks that underlie the coordinated growth and development of the cardiovascular and musculoskeletal systems including identifying signals within and between the major cell types that comprise these organ systems (cardiomyocytes, myofibroblasts, skeletal myoblasts, smooth muscle and endothelial cells). We also study the mechanisms underlying the development of adult onset diseases including hypertension, cardiac hypertrophy, and muscular dystrophy. We use a multi-disciplinary approach that includes the generation of animal models that mirror congenital cardiovascular and musculoskeletal defects in humans and we identify affected signaling networks that govern the aforementioned processes (with a focus on signaling via the extracellular matrix) through cell biology, biochemical, proteomic, and genomic means. We also couple surgical models (transverse aortic banding, carotid ligation, left anterior descending coronary ligation/reperfusion, toxin injection) to genetically manipulated mice to better understand the pathogenesis of cardiovascular and skeletal muscle diseases.