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Insulin-like Growth Factor I
Muscle weakness is a common clinical phenomena observed following prolonged bed rest, surgery, cast immobilization and injury or disease. Although skeletal muscle has an inherent capacity to recover from these maladaptations, the maintenance and recovery of muscle function after disuse can be slow, and in many cases, inefficient and incomplete. Postnatal muscle growth and muscle plasticity occur by two primary mechanisms: increased protein synthesis or the activation of satellite cells.
Previously, growth factors including insulin-like growth factor-I (IGF-I), basic-fibroblast growth factor (bFGF), and nerve growth factor (NGF) were shown to improve muscle regeneration during this preliminary phase of repair. In particular, IGF-I has been shown to play a central role in the promotion of myoblast proliferation and myogenic differentiation in an autocrine/paracrine manner. Based on the importance of IGF-I, our lab coordinated with Drs. Sweeney and Barton from University of Pennsylvania to investigate the potential of virus-mediated (aAAV) gene transfer of IGF-I to guard skeletal muscle from the deleterious impact of immobilization/spinal cord injury and to accelerate the rate of recovery following disuse atrophy.
This study is supported from National Institutes of Health. The ability to protect skeletal muscle during periods of disuse as well as the ability to expedite the patient’s recovery can not only improve the patient’s overall post-injury functional performance, but may increase the patient’s quality of life and chances for living an independent life.
Click on the thumbnails to enlarge the following photos regarding research within the Muscle Physiology Laboratory (below):
