Winnipeg Chapter of the Society for Neuroscience

Dr. Judy Anderson

Judy E. Anderson, PhD
Professor,
Department of Human Anatomy & Cell Science
University of Manitoba
730 William Avenue, Winnipeg, MB R3E 0W3, CANADA
Tel: 204-789-3716 Fax: 204-789-3920
E-mail:
COS profile: http://myprofile.cos.com/judyanderson
U M profile: http://www.umanitoba.ca/faculties/medicine/units/anatomy/anderson.html

See Dr. Anderson's COS profile: http://myprofile.cos.com/judyanderson.

Dr. Judy Anderson from the Department of Human Anatomy and Cell Science at the University of Manitoba has recently discovered a method of triggering muscle growth. Specifically, she has targeted the cells responsible for muscle growth, the so-called satellite cells. Her new discovery takes advantage of normal nitric oxide release in muscle. When something goes wrong or when muscle fibers need to grow, they use nitric oxide to signal satellite cells, located just above muscle fibers, to turn on and begin the growth process.

The new discovery presents numerous possible applications for health care and rehabilitation, treatment of neuromuscular diseases like muscular dystrophy, agriculture and even space travel. People in space tend to experience atrophy very quickly and this new discovery could help to alleviate this problem.

Dr. Anderson's new discovery was just published in the prestigious journal Molecular Biology of the Cell, May 2000.

Figure 8: As cited from Molecular Biology of the Cell 11: 1859-1874; 2000. A model for the process of shear-induced, NO-mediated events that activate satellite cells after skeletal muscle injury. (A)In undamaged muscle with normal contraction and relaxation, thin quiescent satellite cells are demarcated by m-cadherin and contain few organelles. They are interposed between the overlying external lamina and the sarcolemma of a subjacent fiber, and are subject to pulsatile NO released from NOS-I that is anchored to syntrophin. Normally, NO diffuses cylindrically out from the fiber to act on cells and enzymes in the interstitium or is neutralized by red cell hemoglobin in the vessels that wrap each fiber. (B)After sarcolemmal injury, depolarization is not followed by repolarization. A single large contraction produces intense shear between the fiber membrane and external lamina. Shear induces a bolus release of NO that diffuses down its concentration gradient through the satellite cells hugging the fiber. (C)Satellite cells are becoming activated, and begin to enlarge as organelles such as mitochondria hypertrophy. HGF/SF from the damaged fiber is activated and shifts to the c-met receptor on satellite cells. Fibrils hypercontract and damaged segments retract within the external lamina, maintaining shear and NO release and activating satellite cells along the fiber length. The adhesiveness of m-cadherin decreases and the damaged fiber releases proteins including HGF/SF to the interstitium. A released factor like HGF/SF, enters the circulation and can transiently activate distant satellite cells on undamaged muscles, although normal pulsatile NO release will mostly attenuate that response. Capillaries dilate and blood cells extravasate into the interstitium. (D)Fiber segments fully retract and satellite cells become motile precursors as HGF/SF binds to c-met. The external lamina remains as a scaffold for the satellite cells, now surrounded by less adhesive m-cadherin. The precursors may leave the fiber as the sequential expression of early immediate genes, muscle regulatory genes, proliferating cell nuclear antigen and later DNA synthesis begin prior to proliferation.

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