Robert W. Hadley, Ph.D.,
Associate Professor; Director of Graduate Studies
Michigan State, 1987.
Office: MS-371 Chandler Medical Center (0298)
Tel: (859) 257-6556
Teaching and Administrative Interests
Medical Education
MD/PHA 824 (Mechanisms of Disease & Treatment--Pharmacology)
Dental Education
OBI 836 (Dental Pharmacology)
Graduate Education
Director of Graduate Studies
IBS 603 (Cell Biology & Signaling I)
PHA 621 (Principles of Drug Action)
PHA 622 (Molecular Drug Targets & Therapeutics)
Research Interests
My long-term research interests have been centered on the role of ion transporters and ion channels in human disease. Specific interests include the physiological and pathological roles of 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.
Selected Publications
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Eigel, B.N., Gursahani, H. & Hadley, R.W.
The sodium-calcium exchanger (NCX) plays a key role in inducing apoptosis after hypoxia/reoxygenation in
cultured guinea pig ventricular myocytes.
American Journal of Physiology, 287, H1466-H1475. PMID: 15155263.
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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