Stylianos P. Scordilis
Professor of Biological Sciences, Smith College
Ph.D.: State University of New York at Albany Postdoctoral Training: Section on Molecular Cardiology, National Institutes of Health
Our laboratory works on the molecular physiology of skeletal muscle and its gender-specific basis. The molecular response and adaptation of skeletal muscle to unaccustomed exercise is a largely unexplored area of muscle physiology, molecular biology and exercise science. The metabolism of stress proteins in skeletal muscle and their regulation by transcriptional and translational, as well as signal transduction cascade, mechanisms is the focus our lab. This research analyzes the expression of various stress, also know as heat shock, proteins, HSP27, HSP60, the HSP70 and HSP90 families, by eccentrically-biased exercise, that is lengthening contractions, in both human and mouse skeletal muscle in situ, as well as C2C12 cells in culture. Our work indicates that gender differentially regulates the expression of these proteins both immediately post-exercise and long term after an exercise which reparably damages the muscle and, in humans, causes soreness about two days after the insult. Experiments are under way to identify the actual stressor(s) and the effects of the stress protein and mRNA changes. This work utilizes immunoblotting, immunofluorescence, confocal and electron microscopy, along with qRT-PCR and RNAi knockdowns. We are also interested in the regulation of the repeated bout phenomenon. This physiological paradigm is exhibited as a significant attenuation of indirect measures (serum creatine kinase elevations, muscle swelling, soreness, etc.) of muscle damage following a second bout of identical exercise for weeks to months after the exercise. Our work indicates that the cellular stress protein response does not attenuate as do the indirect measures to a second bout of exercise one week after the initial bout. In addition, we have uncovered significant gender-specific differences between exercise-naive male and female mice in both the stress protein response and in the MAPK signaling cascades.