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Physiology




Physiology Home > People > Faculty > Reid
Photo of Michael B. Reid, Ph.D. MICHAEL B. REID, Ph.D.
Chairman
Professor
Ph.D. University of Texas Southwestern Medical Center, 1980
Office: MS-509 Medical Center 0298
Tel: (859) 323-6045
Lab: MS-627
E-mail: mbreid2@uky.edu
Curriculum Vita (pdf)

Our laboratory is studying the biological importance of redox-active signaling molecules – reactive oxygen species (ROS) and nitric oxide (NO) derivatives – as regulators of skeletal muscle function. ROS and NO are continually produced by skeletal muscle cells. These molecules function as second messengers to influence both gene expression and contractile regulation. Under physiological conditions, low levels of ROS and NO are essential for normal homeostasis. But excessive accumulation can perturb cellular processes. For example, during strenuous exercise a rapid build-up of ROS within the tissue contributes to the development of muscular fatigue. Long-term elevation of ROS or NO can have more dire consequences, disrupting excitation-contraction coupling and upregulating genes that promote protein breakdown. Such events are thought to accelerate the weakness, physical inactivity, and premature death that occur in chronic inflammatory diseases, e.g., cancer, AIDS, emphysema, and congestive heart failure. Our research group is working to understand the cellular and molecular mechanisms that underly these problems. We use a variety of experimental approaches that range from cell culture systems to human experimentation, from genetic manipulation to drug intervention. Our long-term goal is to understand the redox biology of skeletal muscle and to identify therapeutic interventions that can protect or improve muscle performance.

Recent Publications:

Li, Y.-P., S.H. Lecker, Y. Chen, I.D. Waddell, A.L. Goldberg, M.B. Reid. TNF-α increases ubiquitin-conjugating activity in skeletal muscle by up-regulating UbcH2/E2-20k. FASEB J 17: 1048-1057, 2003.

Reid, M.B., J. Lännergren, and H Westerblad. Respiratory and limb muscle weakness induced by TNF-α: involvement of muscle myofilaments. Am. J. Resp. Crit. Care Med. 166: 479-484, 2002.

Reid, M.B. and W.J. Durham. Generation of reactive oxygen and nitrogen species in contracting skeletal muscle: potential impact on aging. Ann. N.Y. Acad. Sci. 959: 108-116, 2002.

Reid, M.B., and Y.-P. Li. Cytokines and oxidative signaling in skeletal muscle. Acta Physiol. Scand. 171: 225-232, 2001.

Reid, M.B. Invited review: Redox modulation of skeletal muscle contraction: What we know and what we don’t. J. Appl. Physiol. 90: 724-731, 2001.

Other Publications

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