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Increased expression of myostatin and its receptor, activin RIIb, after 14 day hindlimb unloading in the mouse.      B.J. Greybeck¹, D.L. Allen², A.M. Hanson¹, V.L. Ferguson³, L. S. Stodieck^{1     1}Department of Aerospace Engineering Sciences, and ²Integrative Physiology, and ³Mechanical Engineering at the University of Colorado

   The molecular mechanisms behind space flight induced muscle atrophy remain little understood.  One of these mechanisms, Myostatin (MSTN), is a member of the Transforming Growth Factor (TGF)-β family of proteins which binds to the activin RIIB (ActRIIb) receptor and greatly inhibits muscle growth. In the present work we examined the effects of 14 days of hindlimb unloading on mRNA levels of MSTN and ActRIIb in mice. It was hypothesized that there would be an upregulated mRNA levels of myostatin and its receptor ActRIIb after 14 days of hindlimb suspension of mice. METHODS: RNA was isolated from 6 cage control and 6 hindlimb unloaded mice tibialis anterior muscles and quantitative real-time PCR was used to quantify MSTN and ActR2B mRNA levels. RESULTS: There was increased expression of both myostatin and ActRIIb mRNA after 14 days of unloading with decreased wet muscle mass. These data suggest that myostatin and its receptor may contribute to spaceflight and hindlimb unloaded muscle atrophy.