Associate Chair for Graduate Studies
Office: BMH 3031
Phone: (519) 888-4567, ext. 38131
Fax: (519) 885-0470
The primary focus of my research program is to study the biochemical and molecular mechanisms regulating cell death processes (i.e., apoptosis and autophagy) in tissues, particularly skeletal muscle. Specifically, my laboratory is interested in how factors such as mitochondrial function and oxidative stress influence cell death signaling in response to injury/stress, aging, and disease. My laboratory is also currently investigating the role of apoptosis repressor with caspase recruitment domain (ARC) on skeletal muscle development and apoptosis. In addition, my research explores the potential benefits of physical activity on cell death processes in both health and disease.
It is now well recognized that cells can undergo several different forms of cell death. “Programmed cell death” has traditionally been used to describe apoptosis (or type I cell death). Apoptosis is a highly conserved cell death mechanism that allows multi-cellular organisms to maintain tissue and cellular homeostasis. Apoptotic signaling is now well accepted to play a significant role in the pathogenesis of tissue dysfunction and disease. Autophagy is a cellular degradation mechanism that aids in the removal of cytoplasmic contents such as macromolecules and organelles, which also participates in cell death (type II cell death). A wealth of literature has established dysregulation of autophagic processes as a key mechanism in the pathogenesis of disease. Apoptotic and autophagic processes also play a significant role in skeletal muscle wasting and dysfunction, but are also critical for normal skeletal muscle development.
Physical activity plays an important role in the management and prevention of disease. It is well established that exercise can alter a number of intracellular and extracellular signaling pathways. Recent work has demonstrated that exercise can influence cell death pathways in a variety of tissues, including skeletal muscle. In particular, regular physical activity can promote a “pro-survival” environment and decrease apoptotic signaling. Collectively, the evidence suggests that lifestyle modifications may preserve cellular function during aging and disease by altering apoptotic signaling and cell death processes.
For further information please visit the Muscle Biology & Cell Death Laboratory website.
Graduate supervision and student opportunities
I am currently accepting applications for student opportunities in the following areas:
- Research volunteer
- Undergraduate thesis
- MSc thesis
- PhD thesis
- Postdoctoral fellowship
Please email me to discuss current available opportunities.
Teaching, expertise, tools and technologies
- Skeletal muscle biology
- Skeletal muscle disease
- Exercise physiology
- Cell and molecular biology
- Cell culture
- Animal models
- Cellular imaging
KIN 406: Physiology of Skeletal Muscle Aging & Disease
KIN 606: Molecular Basis of Disease
McMillan, E.M., Paré, M.-F., Baechler B.L., Graham, D.A., Rush, J.W.E., Quadrilatero, J. Autophagic signaling and proteolytic enzyme activity in cardiac and skeletal muscle of spontaneously hypertensive rats following chronic aerobic exercise. PLoS ONE, 2015, 10: e0119382.
Mitchell, A.S., Smith, I.C., Gamu, D., Donath, S., Tupling, A.R., Quadrilatero, J. Functional, morphological, and apoptotic alterations in skeletal muscle of ARC deficient Mice. Apoptosis, 2015, 20: 310-326.
Campbell, T.L., Mitchell, A.S. McMillan, E.M., Bloemberg, D., Pavlov, D., Messa, I., Mielke, J.G., Quadrilatero, J. Effect of a 16 week high fat diet on rat skeletal muscle autophagic and apoptotic signaling. Experimental Biology and Medicine, 2015, 240: 657-668.
Bloemberg, D. and Quadrilatero, J. Mitochondrial pro-apoptotic indices do not precede the transient caspase activation associated with myogenesis. Biochimica et Biophysica Acta - Molecular Cell Research, 2014, 1843: 2926-2936.
McMillan, E.M. and Quadrilatero, J. Autophagy is required and protects against apoptosis during myoblast differentiation. Biochemical Journal, 2014, 462: 267-277.
Bloemberg, D. and Quadrilatero, J. Rapid determination of myosin heavy chain expression in rat, mouse, and human skeletal muscle using multicolor immunofluorescence analysis. PLoS ONE, 2012, 7: e35273.
Quadrilatero, J., Alway, S.E., Dupont-Versteegden, E.E. Skeletal muscle apoptotic response to physical activity: Potential mechanisms for protection. Applied Physiology, Nutrition, and Metabolism, 2011, 36: 608-617.