Kerry S. McDonald, PhD
My research focuses on the cellular and molecular mechanisms involved in the regulation of striated muscle contraction and how these regulatory processes are altered by disease and other physiological stresses such as exercise. To address these questions, my lab takes a multi-faceted approach incorporating tissue, cellular, and molecular preparations. For many of our experiments,we utilize preparations of single skeletal muscle fibers or single cardiac myocytes from which the sarcolemma has been chemically removed while the myofilaments remain intact so that mechanical measurements can be made. In these preparations the chemical environment surrounding the myofilaments can be manipulated, allowing precise control of the cell's level of activation. Another advantage of these preparations is that the protein composition from these cells can be experimentally manipulated as well as quantified after mechanical measurements.
Currently, my laboratory is investigating the factors that regulate power output capacity of single cardiac myocytes, which is a physiological variable that is essential for the heart to move blood throughout the circulatory system. We are currently examining how power output is regulated by factors such as contractile protein isoforms, activator calcium, sarcomere length, and phosphorylation states of myofibrillar proteins. My research program also provides a means for trainees in our department to examine either the mechanical behavior or altered biochemical properties of striated muscle in response to various models of muscle disease or altered muscle activity. For example, we currently are collaborating with Dr. Harold Laughlin to examine whether cardiac muscle regulatory proteins, phosphorylation states of these proteins, and contractile properties of cardiac myocytes are altered in response to exercise. We are also collaborating with Dr. Joe Kornegay and Dr. Casey Childers in studies that examine mechanical changes of skeletal muscle in response to a canine model of Duchenne's muscular dystrophy.
- B.A. in biology, Benedictine College, Received Ph.D. in biology, Marquette University
- NIH sponsored postdoctoral fellow, University of Wisconsin
- Joined Department in 1997
- Member of The Biophysical Society and The American Physiological Society
- Reviewer for several physiological journals
- Research currently funded by NIH and AHA
- Winner of the 2001 Dorsett L. Spurgeon M.D. Distinguished Medical Research Award, 2001
- NIG Independent Scientist Award (2003-2004)
- Korte, F.S., E. Mokelke, M. Sturek and K.S. McDonald. Endurance exercise training enhances left ventricular function in diabetic dyslipidemic pigs: correlation with changes in cardiac myofibrillar proteins. J Appl Physiol (in press).
- Hinken, A.C. and K.S. McDonald. Inorganic phosphate speeds loaded shortening in skinned cardiac myocytes. Am. J. Physiol. 287:C500-C507, 2004.
- Childers, M.K. and K.S. McDonald. Skletal muscle fiber force and power increase with regulatory light chain phosphorlation. Muscle & Nerve. 29:313-317, 2004.
- Korte, F.S., K.S. McDonald, S.P. Harris, and R.L. Moss. Loaded shortening, power output and rate of force redevelopment are increased with knockout of cardiac myosin binding protein-C. Circ. Res. 93:752-758, 2003.
- McDonald, K.S. and T.J. Herron. It takes "heart" to win: What makes the heart powerful? New Physiol. Sci. 17:185-190, 2002.
- Herron, T.J. and K.S. McDonald. Small amounts of alpha-myosin heavy chain isoform expression significantly increase power output of rat cardiac myocytes fragments. Circ. Res. 90:1150-1152, 2002.
- Herron, T.J., F.S. Korte and K.S. McDonald. Power output is increased following phosphorylation of myofibrillar proteins in skinned rat cardiac myocytes. Circ. Res. 89:1184-1190, 2001.
- McDonald, K.S. Ca2+ dependence of loaded shortening in rat skinned cardiac myocytes and skeletal muscle fibres. J. Physiol. (Lond.) 525:169-181, 2000.