The research interest in my laboratory is the role of calcium ions in the pathogenesis of cardiac disease. The development of heart disease is a complicated process, involving many alterations at the molecular, cellular and whole animal levels. It is well known that calcium ions play very important roles in normal physiology of the heart. Calcium is the key determinant of the contractility of cardiac myocytes and thus the heart contractility. Recently, roles of calcium as a signaling ion have been widely studied. Specifically in the heart, calcium plays roles in cardiac myocyte hypertrophy, death, arrhythmogenic activities and remodeling. However, it is not fully explored that how Ca2+ signaling is encoded among constant change of cytosolic Ca2+ during each heart beat. Currently, I am studying the roles of the L-type calcium channel in heart disease progression with a transgenic mouse model cardiac specifically overexpressing the L-type calcium channel beta2a subunit in collaboration with Drs. Steven R. Houser and Jeffrey Molkentin’s groups with the support from NIH/NHLBI and American Heart Association. The roles of calcium ions in the development of cardiac failure, arrhythmia, hypertrophy, myocyte death, and turnover are under exploration in this model. Techniques used in my laboratory range from molecules to whole animals and include molecular biology, myocyte isolation and culture, electrophysiology, intracellular ion measurements, histology, immunocytochemistry, echocardiography, animal surgeries (transaortic constriction, osmotic minipump implantation, coronary artery ligation), and telemetrical ECG recording
