Michael J. Rovetto , Ph.D.

Professor rovettom@health.missouri.edu

Research Interests 
Control of Myocardial Energy Production
Transport of Purine Nucleosides
Regulation of Myocardial Contractile Activity in disease states of:
DiabetesI Ischemia
Hypothyroidism Muscular Dystrophy

Models Utilized for Studies 
Isolated Perfused Rat and Mice Hearts
Used to assess metabolic and contractile activity
Isolated Cardiac Muscle Cells
Used to determine metabolic and transport activities
Cultured Cardiac Muscle Cells
Used to study long term regulation of metabolic activity

Research Projects 
Myocardial ischemia caused by inadequate blood flow to the heart muscle leads to purine loss from cells. The extent to which they are lost is directly related to recovery of mechanical function upon restoration of blood flow to the heart. Thus, decreased purine levels and decreased ability of the heart to perform useful work are coupled. I am interested in determining what controls rates of transport of purines into and out of cells and how this process can be altered to enhance the energy state of the heart.
 
Related to these studies are investigations of how the cardioprotective substance, fructose phosphate crosses heart cell membranes. These studies are done in collaboration with Dr. Christopher Hardin.

Membrane transport of glucose also is of interest and of naturally occurring and genetically-induced animal models that lead to diabetes and/or hypertension are used to understand the role of the renin-angiotensin system in the pathologic consequences of diabetes & hypertension. These studies are done in association with Drs. James Sowers and Craig Stump, department of medicine and the Truman V.A. hospital.
 
A model of hypothyroidism is used to alter the contractile activity of myocardial muscle in order to determine how specific changes in the contractile protein myosin affect the rate of force development by isolated muscle cells and intact heart. This is a collaborative research project with Dr. Kerry McDonald.
 
A similar investigation to that in hypothyroidism, but in hearts from genetically altered mice that exhibit traits of an inherited form of muscular dystrophy, are being carried out in collaboration with Drs. Joe Kornegy and Casey Childers college veterinary medicine and department of physical and rehabilitation medicine.

Pertinent publication: Hardin, CD et al. Myocardial metabolism of exogenous FDP is consistent with transport by a dicarboxylate transporter. Am J Physiol.Heart Circ Physiol 281:H2654, 2001.

Professional Background

• Received Ph.D. in physiology, University of Virginia
• Completed postdoctoral studies at Hershey Medical Center
• Joined Department in 1980
• Elected member/fellow of several societies including The American Physiological Society, The Biophysical Society, and The American Heart Association
• Served on several NIH study sections and was a member of the Cardiovascular and Renal Study Section
• Past reviewer on the Veterans Administration Cardiovascular Merit Review Board
• Served on the editorial boards of The American Journal of Physiology and Circulation Research
• Past member of the editorial board of The International Journal of Purine and Pyrimidine Research
• Previous NIH Research Career Development Awardee Research in heart metabolism
• Has been continuously funded by NIH grants since 1975

Selected Publications

• Ford, D.A. and M.J. Rovetto. Rat cardiac myocyte adenosine transport and metabolism. Am. J. Physiol. 252:H54-H63, 1987.
• Sunnergren, K.P. and M.J. Rovetto. Myocyte and endothelial cell injury with ischemia reperfusion in isolated rat hearts. Am. J. Physiol. 252:H1211- H1217, 1987.
• Hale, C.C., S.B. Kleiboeker, C.G. Carlton, M.J. Rovetto, C.Y. Jung and H.D. Kim. Eviden ce for high molecul ar weight Na-Ca exchan ge in cardiac sarcole mmal vesicles. J. Membr. Biol. 106:21 1-218, 1988.
• Hale, C.C., C.G. Carlton and M.J. Rovetto. Adenosine uptake in cardiac sarcolemmal vesicles. Int. J. Purine Pyrimid ine Researc h 1:1-6, 1990.
• Dale, W.E., C.C. Hale, H.D. Kim and M.J. Rovetto. Myocardial glucose utilization. Failure of adenosine to alter it and inhibition by the adenosine analogue N6-(L-2- phenylisopropyl) adenosine. Circ. Res. 69:791-799, 1991.
• Geisbuhler, T.P., T.L. Schwager and M.J. Rovetto. Guanosine metabolism in adult rat cardiac myocytes: inhibition by acyclovir and analysis of a metabolic pathway. J. Mol. Cell. Cardiol. 24:683-690, 1992.

Methodology/Techniques