Molecular adaptations of skeletal muscle and cardiac muscle in the hibernating thirteen-lined ground squirrel, Spermophilus tridecemlineatus.
Many small mammals face severe problems during the winter – little or no food supply and yet huge energy costs for keeping their bodies warm. To escape these problems, they hibernate, entering states of deep torpor where metabolic rate falls to just 2-4% of normal and body temperature falls to near 0°C. Remarkably, skeletal muscle sustains cell size and strength despite extended periods of disuse during torpor whereas cardiac muscle actually promotes cell growth (hypertrophy) to support the stronger cardiac contractions needed in the cold. Despite overall suppression of transcription and translation during hibernation, the present research identified and analyzed selected muscle genes and their products that were up-regulated during torpor in striated muscle of thirteen-lined ground squirrels (Spermophilus tridecemlineatus). These changes in myocyte enhancer factor-2 (MEF2a, MEF2c) transcription factor levels as well as altered expression of selected downstream targets (e.g. glucose transporter 4, myogenic differentiation protein) aid skeletal and cardiac muscle in meeting metabolic challenges associated with hibernation. MEF2 transcription factors were significantly elevated at various points in the torpor-arousal cycle suggesting a significant role for MEF2-mediated gene transcription in the selective adjustment of striated muscle proteins. Muscle plasticity in the hibernator was also evidenced by torpor-responsive changes in the levels of important contractile (troponin I, α/β-tropomyosin), sarcomeric (myomesin) and cytoskeleton proteins (desmin, andvimentin). These data provides new insights into muscle remodeling during hibernation and the role of selected genes/proteins in balancing programs of atrophy, stasis andmyogenesis.