Kerry S. McDonald, PhD
My work focuses on understanding the cellular and molecular mechanisms involved in the regulation of striated muscle contraction and ways that these processes may be altered by disease and other physiological stresses such as ischemia and exercise training. To address these questions, I have taken multi-faceted approaches incorporating tissue, cellular, and molecular preparations. For many of my experimental measurements, I utilize preparations of single cardiac myocytes or skeletal muscle fibers from which the sarcolemma has been chemically removed. While these preparations are difficult to use, they present important advantages in designing experimental protocols. For example, the structure of the myofilaments remains intact so mechanical measurements can be made without confounding influences of extracellular connective tissue. Another advantage of these preparations is the chemical environment surrounding the myofilaments can be manipulated, allowing precise control of the cell's level of activation. Finally, protein composition and phosphorylation state of the myofibrils can be experimentally manipulated. Currently, my laboratory is investigating the factors that regulate the capacity of single cardiac myocytes to perform work, a physiological variable that is essential for the heart to move blood throughout the circulatory system. We are currently examining how work capacity of cardiac myocytes is regulated by factors such as contractile protein isoforms, activator calcium, sarcomere length, and phosphorylation states of myofibrillar proteins. My research program 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 are currently examining myofilament changes during the progression of hypertensive heart disease. We also examine myocyte changes associated with aging (in collaboration with Dr. Timothy Domeier), large animal hypertension and exercise (with Dr. Craig Emter) and mouse models of altered myocyte signaling (with Dr. Maike Krenz and Dr. Chris Baines).
- 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
- Research currently funded by NIH
- Served on NIH Cardiac Contractility, Hypertrophy, and Failure study section from 2006-2014
- Hanft, L.M., M.L. Greaser, and K.S. McDonaldArch Biochem & Biophys, 2013.
- Hanft, L.M., B.J. Biesiadecki, and K.S. McDonald. Length dependence of striated muscle force generation is controlled by phosphorylation of cTnI at serines 23/24. J Physiol (Lond).591:4535-4547, 2013.
- Marshall K.D., B.N. Muller, M. Krenz, L.M. Hanft, K.S. McDonald, K.C. Dellsperger, C.A. Emter. Heart failure with preserved ejection fraction: chronic low-intensity interval exercise training preserves myocardial oxygen balance and diastolic function. J Appl Physiol. 114:131-147, 2013.
- McDonald, K.S., L.M. Hanft, T.L. Domeier, and C.A. Emter. Length and PKA dependence of force generation and loaded shortening in porcine cardiac myocytes. Biochemistry Research International. 2012:371415, 2012.
- Hinken A.C., L.M. Hanft, S.B. Scruggs, S. Sadayappan, J. Robbins, R.J. Solaro, and K.S. McDonald. Protein kinase C depresses cardiac myocyte power output and attenuates myofilament responses induced by protein kinase A. J Muscle Res & Cell Motility.33:439-448, 2012.
- Hanft, L.M. and K.S. McDonald. Length-dependence of force generation exhibit similarities between rat cardiac myocytes and skeletal muscle fibres J Physiol (Lond). 588:2891-2903, 2010.