James D. Marsh, M.D., F.A.H.A, F.A.C.P. is Chair of the Department of Internal Medicine and a molecular as well as clinical cardiologist. His research laboratory has a longstanding interest in alterations in cardiac function with early development and also with aging. Studying cardiac myocytes in culture, his laboratory has elucidated age-related alteraions in expression of genes and proteins critical to excitation-contractioncoupling, including proteins comprising the l-type calcium channel, beta adrenergic receptor, and the Na/Ca exchanger. In collaboration with Kish Golden PhD he has recently been studying the mecahnisms by which the aging male heart differs from the female heart, and how contractile performance declines with age-related decline in testosterone levels. Using both in vitro and in vivo approaches in the rat model, Golden, Marsh and collaborators have discovered that the normal physiological decline in androgens or pathological decline in androgens produces depressed cardiac contractile function due to altered transcription of genes encoding calcium regulating proteins and myosin isoform switching. These effects are reveresed by androgen supplementation.

Selected Publications

Golden KL, Marsh JD, Jiang Y. castration reduces mRNA levels for calcium regulatory proteins in rat heart. Endocrine 19(3):339-344, 2002.

Golden KL, Marsh JD, Jiang Y, Brown T, Moulden J. Gonadectomy of adult male rats reduces contractility of isolated cardiac myocytes. Am J Physiol Endocrinal Metab. 285:E449-E453, 2003.

Golden KL, Marsh JD, Jiang Y, Moulden J. Gonadectomy alters myosin heavy chain composition in isolated cardiac myocytes. Am J Physiology. Submitted 2004.

Golden KL, Marsha JD, Jiang Y. Testosterone regulates mRNA levels of calcium regulatory proteins in cardiac myocytes. Submitted 2004