Diane L.M. Hickson-Bick, Ph.D.
1993, Baylor College of Medicine
UT-Houston Medical School
Pathology and Laboratory Medicine
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Diane L.M. Hickson-Bick, Ph.D. 1993, Baylor College of Medicine UT-Houston Medical School |
Research Interests: Cardiac energy metabolism; apoptosis; cardiac ischemia and shock
The goal of the research in my laboratory is aimed at understanding the control of cardiac metabolism in health and disease. Cardiomyocytes are terminally differentiated cells and cell death leads to a functional loss of these cells. My laboratory is interested in the loss of cardiomyocytes by programmed cell death, or apoptosis, particularly with respect to the events initiated within the mitochondrion. Mitochondrial changes, including the release of cytochrome c and the loss of the mitochondrial specific lipid, cardiolipin, have been implicated as early events in apoptosis initiated by diverse stimuli. Of particular interest in my laboratory is the role that cardiolipin synthesis and metabolism has on the susceptibility of the cardiomyocyte to apoptosis.
My laboratory is also interested in the role bacterial lipopolysaccharide (LPS) on cardiac function and metabolism. LPS, a component of bacterial cell walls, induces multiple organ responses and can lead to ultimately to toxic shock and death. One of the clinically important sequellae of LPS exposure is damage to the heart. The role of apoptosis in this cardiac damage is not clear and we seek to integrate our understanding of the induction of apoptosis with the immune response that LPS stimulates.
A tutorial in my laboratory would provide experience in the basic biochemistry and molecular biology of cardiac mitochondrial phospholipid synthesis and remodeling; analysis of apoptosis by enzymatic and deconvolution microscopic techniques. Experience will also be gained in primary cell culture; viral infection; general protein analysis including Western Blot, RT-PCR, electromobility shift assays and lipid analysis.
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Hickson-Bick, D.L.M., Buja, L.M. and. McMillin, J.B. (2000) Palmitate mediated alterations in the fatty acid metabolism of rat neonatal cardiac myocytes. Journal of Molecular and Cellular Cardiology 32:511-519.
Sparagna, G. and Hickson-Bick D.L.M. (1999). Cardiac fatty acid metabolism and the induction of apoptosis. American J. Med Sciences 318, 15-21.
Sparagna, G.C., Hickson-Bick D.L.M., Buja, L.M. and McMillin, J.B. (2000) A metabolic role for mitochondria in palmitate-induced cardiac myocyte apoptosis. Am. J Physiol Heart Circ Physiol. 279: H2124-H2132.
Sparagna, G. Hickson-Bick, D.L., Buja, L.M. and McMillin, J.B. (2001) Fatty acid induced apoptosis in neonatal cardiomyocytes: Redox signaling. Antioxidants and Redox Signaling 3:71-79.
Pownall, H.J., Bick, D.H., Kimball, K.T., Zoch, D., Ballantyne, C.M. (2000) Acute effects of alcohol on the turnover of very low density (VLDL) apolipolipoproteins B-100 in normolipidemic subjects. Moderate Alcohol Consumption and Cardiovascular Disease. (R. Poaletti et al, Eds). Kluwer Academic Publishers and Fondazione Giovanni Lorenzini, Netherlands. P 47-52.
Shelat, H.S., Liu, T-J., Hickson-Bick, D.L., Barnhart, M.K., Vida, T., Dillard, P.M., Willerson, J.T., Zoldhelyi, P.(2001) Growth suppression of human vascular smooth muscle cells by gene transfer of the transcription factor E2F-1. Circulation; 103:407-414.
Hickson-Bick, D.L.M., Sparagna,G.C., Buja L.M., and McMillin, J.B.. (2002) Palmitate-induced apoptosis in neonatal cardiomyocytes is not dependent on the generation of reactive oxygen species. Am. J Physiol Heart Circ Physiol ; 282: H656-H664.
Sparagna, G.C., Jones, C.E., Hickson-Bick, D.L.M. (2004) Attenuation of fatty acid-induced apoptosis by low dose alcohol in neonatal rat cardiomyocytes. Am. J Physiol Heart Circ Physiol; 287:H2209-H2215.
Program Affiliation:
Program in Molecular Pathology