Physiology

JENNIFER STEVENSON MOYLAN, Ph.D. Assistant Professor Ph.D. University of Arizona, 1994 Office: MS-607A Medical Center 0298 Tel: (859) 323-2721 E-mail: jennifer.moylan@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:

Ferreira LF, Moylan JS, Gilliam LA, Smith JD, Nikolova-Karakashian M, Reid MB. (2010) Sphingomyelinase stimulates oxidant signaling to weaken skeletal muscle and promote fatigue. Am J Physiol Cell Physiol. 2010 Jun 2. [Epub ahead of print].

Chambers MA, Moylan JS, Reid MB. (2009) Physical inactivity and muscle weakness in the critically ill. Crit Care Med. 2009 Oct;37(10 Suppl):S337-46.

Gilliam LA, Ferreira LF, Bruton JD, Moylan JS, Westerblad H, St Clair DK, Reid MB. (2009) Doxorubicin acts through tumor necrosis factor receptor subtype 1 (TNFR1) to cause dysfunction of murine skeletal muscle. J Appl Physiol. Sep. [Epub ahead of print].

Li W, Moylan JS, Chambers MA, Smith J, Reid MB. (2009) Interleukin-1 stimulates catabolism in C2C12 myotubes. Am J Physiol Cell Physiol. 297(3):C706-14.

Chambers MA, Moylan JS, Smith JD, Goodyear LJ, Reid MB. (2009) Stretch-stimulated glucose uptake in skeletal muscle is mediated by reactive oxygen species and p38 MAP-kinase. J Physiol. 587:3363-73.

Moylan JS, Smith JD, Chambers MA, McLaughlin JT, Reid MB. (2008) TNF induction of atrogin-1/MAFbx mRNA depends on Foxo4 expression but not AKT-Foxo1/3 signaling. Am J Physiol Cell Physiol 2008 295:C986-93.

Hardin BJ, Campbell KS, Smith JD, Arbogast S, Smith JL, Moylan JS, Reid MB. TNF-{alpha} Acts Via TNFR1 and Muscle-Derived Oxidants to Depress Myofibrillar Force in Murine Skeletal Muscle. J Appl Physiol. 2008 104(3):694-9.

Other Publications