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Quadrilatero, Joe

Joe Quadrilatero photo

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Research:

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.

Key Publications:

  1. 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(4): e35273.
  2. Dam, A.D., Mitchell, A.S., Rush, J.W.E., Quadrilatero, J. Elevated apoptotic signaling in skeletal muscle following glutathione depletion. Apoptosis, 2012, 17: 48-60.
  3. 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.
  4. McMillan, E.M. and Quadrilatero, J. Differential apoptosis-related protein expression, mitochondrial properties, proteolytic enzyme activity, and DNA fragmentation between skeletal muscles. American Journal of Physiology – Regulatory, Integrative & Comparative Physiology, 2011, 300, R531-R543.
  5. Quadrilatero, J. and Bloemberg, D. Apoptosis repressor with caspase recruitment domain is dramatically reduced in cardiac, skeletal, and vascular smooth muscle during hypertension. Biochemical and Biophysical Research Communications, 2010, 391, 1437-1442.
  6. Quadrilatero, J., Bombardier, E., Norris, S.M., Talanian, J.L., Palmer, M.S., Logan, H.M., Tupling, A.R., Heigenhauser, G.J.F, Spriet, L.L. Prolonged moderate intensity aerobic exercise does not alter apoptotic signaling and DNA fragmentation in human skeletal muscle. American Journal of Physiology - Endocrinology and Metabolism, 2010, 298, E534-E547.
  7. Quadrilatero, J. and Rush, J.W. Evidence for a pro-apoptotic phenotype in skeletal muscle of hypertensive rats. Biochemical and Biophysical Research Communications, 2008, 368, 168-174.
  8. Quadrilatero, J. and Rush, J.W. Increased DNA fragmentation and altered apoptotic protein levels in skeletal muscle of spontaneously hypertensive rats. Journal of Applied Physiology, 2006, 101, 1149-1161.
  9. Quadrilatero, J. and Hoffman-Goetz, L. N-Acetyl-L-cysteine protects intestinal lymphocytes from apoptotic death following acute exercise in adrenalectomized mice. American Journal of Physiology – Regulatory, Integrative & Comparative Physiology, 2005, 288, R1664-1672.
  10. Quadrilatero, J. and Hoffman-Goetz, L. N-Acetyl-L-cysteine inhibits exercise-induced intestinal lymphocyte apoptotic protein alterations. Medicine & Science in Sports & Exercise, 2005, 37, 53-56.
  11. Quadrilatero, J. and Hoffman-Goetz, L. N-Acetyl-L-cysteine prevents exercise-induced intestinal lymphocyte apoptosis by maintaining intracellular glutathione levels and reducing mitochondrial membrane depolarization. Biochemical and Biophysical Research Communications, 2004, 319, 894-901.