Michael Massett, Ph.D.

Michael Massett, Ph.D. Research Assistant Professor Michael_Massett@urmc.rochester.edu Primary Appointment: Department of Medicine in the Aab Cardiovascular Research Institute University of Rochester School of Medicine and Dentistry 601 Elmwood Ave, Box 679 MRBX - Rm. 2.11 Rochester, New York 14642 Phone: (585) 273-1493 Fax: (585) 276-1914

Dr. Michael Massett earned his Ph. D. in Exercise Science from The University of Iowa in 1997. His post-doctoral training was done in Gabor Kaley’s laboratory at New York Medical College. Dr. Massett joined the Center for Cardiovascular Research at the University of Rochester in 2000, where he completed his post-doctoral training in Dr. Bradford Berk’s laboratory. Currently, he is a Research Assistant Professor in Medicine in the Center for Cardiovascular Research. Dr. Massett’s research interests include the mechanisms underlying the peripheral vascular adaptations to exercise and the relationship between acute and chronic exercise and the progression and treatment of cardiovascular disease.

Research Overview

Exercise training elicits a number of beneficial effects that can reduce the risk of chronic diseases including hypertension, atherosclerosis, type 2 diabetes, and osteoporosis. However, both intrinsic exercise capacity and the response to exercise training are highly variable, such that some individuals may not respond to exercise training. Although many of the phenotypic traits associated with exercise training are well known, the genetic factors determining the response to exercise are poorly understood. Thus, identifying the genetic factors modulating the adaptations to exercise may provide insight into the prevention and treatment of many of these diseases. The overall objective of my research is to identify biological mediators of these adaptations that may be utilized in the future as new targets for pharmacological treatment, gene therapy, or other interventions for the treatment of chronic diseases such as atherosclerosis or diabetes. To address this question, I am using two strategies: 1) comparison of exercise capacity and training responses in several inbred mouse strains and 2) candidate gene approach using transgenic mice.

To control the genetic and environmental factors that contribute to responses to acute exercise and exercise training, I have developed an exercise-training paradigm for mice. Recently completed experiments characterizing the response to exercise training in inbred and F1 hybrid mouse strains demonstrate that there are large strain-dependent differences in training responses among inbred mouse strains. In addition, there were contrasting responses to training in reciprocal F1 hybrid strains implying that variation in mitochondrial proteins and function may contribute to strain-dependent differences in training responses. Future research plans include using genetic/genomic approaches and biochemical techniques to identify quantitative trait loci (QTL) and differences in gene/protein expression that contribute to variation in training adaptations.

I am also using a candidate gene approach to identify genetically defined modifiers of the exercise response. Although maximal exercise capacity and sub-maximal endurance exercise performance are complex polygenic traits, several candidate genes contributing to improved exercise capacity have been proposed, including angiotensin converting enzyme (ACE) and angiotensinogen. Therefore, this aspect of my research addresses the hypothesis that the responses to exercise training are modulated by the renin-angiotensin system. This project utilizes transgenic mice expressing different copy numbers of the angiotensinogen gene to identify the interaction between the renin-angiotensin system and the adaptations to exercise training.

Recent Publications

1. Massett, M. P., S. J. Lewis, H. M. Stauss, and K. C. Kregel. Vascular reactivity and baroreflex function during hyperthermia in conscious rats. Am. J. Physiol. Regulatory, Integrative Comp. Physiol. 279: R1282-R1289, 2000.
2. Massett, M. P., Z. Ungvari, A. Csiszar, G. Kaley, and A. Koller. Differential role of PKC and MAP kinases in myogenic and agonist-induced constriction of skeletal muscle arterioles. Am. J. Physiol. Heart Circ. Physiol. 283: H2282-H2287, 2002.
3. Korshunov, V.A., M. P. Massett, R.M. Carey, and B.C. Berk. Role of angiotensin converting-enzyme and neutral endopeptidase in flow-dependent remodeling. J. Vasc. Res. 41: 148-156, 2004.
4. Massett, M. P., and B.C. Berk. Strain-dependent differences in responses to exercise training in inbred and hybrid mice. In Press Am. J. Physiol. Regul.Integr. Comp. Physiol.