Robert W. Hadley, Ph.D.,
Associate Professor; Director of Graduate Studies
Michigan State, 1987.
Office: MS-371 Chandler Medical Center (0298)
Lab: (859) 323-3287
Tel: (859) 257-6556
My long-term research interests are centered on the role of ion transporters and ion channels in human disease. Current studies in my lab are focused on the sodium-calcium exchanger, a family of membrane proteins that play a critical role in mediating calcium signaling in excitable cells. Malfunction of the sodium-calcium exchanger is thought to play a key role in causing the death of neurons and cardiac myocytes during ischemic stroke and myocardial infarction. Expression of the sodium-calcium exchanger is also enhanced by such conditions as cardiac hypertrophy and heart failure, a phenomenon that may promote sudden cardiac death via cardiac arrhythmias, and ischemic cell death through necrosis and apoptosis. The current experimental objectives of my lab include defining the mechanisms by which sodium-calcium exchanger function or expression is regulated. For example, recent studies have implicated elevated oxidative stress as a key regulator of the sodium-calcium exchanger in various disease states.
Selected Publications
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Eigel, B.N., Gursahani, H. & Hadley, R.W.
The sodium-calcium exchanger (NCX) can initiate apoptosis following hypoxia/reoxygenation in adult
cultured guinea pig ventricular myocytes.
American Journal of Physiology, in press.
Eigel, B.N., Gursahani, H. & Hadley, R.W.
Reactive oxygen species activate sodium-calcium exchange-mediated calcium overload following
hypoxia/reoxygenation in guinea pig ventricular myocytes.
American Journal of Physiology 286, H955-H963.
Eigel, B.N. & Hadley, R.W.
Antisense inhibition of Na+/Ca2+ exchange during anoxia/reoxygenation in ventricular myocytes.
American Journal of Physiology 281, H2184-H2190.
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