4.4 Article Proceedings Paper

HINDLIMB SKELETAL MUSCLE FUNCTION IN MYOSTATIN-DEFICIENT MICE

期刊

MUSCLE & NERVE
卷 43, 期 1, 页码 49-57

出版社

WILEY
DOI: 10.1002/mus.21796

关键词

muscle weakness; muscle weight; myostatin deficiency; peak tetanic force; sex differences

资金

  1. NCRR NIH HHS [T32 RR007004] Funding Source: Medline
  2. NICHD NIH HHS [HD058834, R21 HD058834, R21 HD058834-02] Funding Source: Medline
  3. EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [R21HD058834] Funding Source: NIH RePORTER
  4. NATIONAL CENTER FOR RESEARCH RESOURCES [T32RR007004] Funding Source: NIH RePORTER

向作者/读者索取更多资源

Absence of functional myostatin (MSTN) during fetal development results in adult skeletal muscle hypertrophy and hyperplasia. To more fully characterize MSTN loss in hind-limb muscles, the morphology and contractile function of the soleus, plantaris, gastrocnemius, tibialis anterior, and quadriceps muscles in male and female null (Mstn (+/+)), heterozygous (Mstn(+/-)), and wild-type (Mstn(+/+)) mice were investigated. Muscle weights of Mstn(-/-) mice were greater than those of Mstn(+/+) and Mstn(+/-) mice. Fiber cross-sectional area (CSA) was increased in female Mstn(-/-) soleus and gastrocnemius muscles and in the quadriceps of male Mstn(-/-) mice; peak tetanic force in Mstn(-/-) mice did not parallel the increased muscle weight or CSA. Male Mstn(-/-) muscle exhibited moderate degeneration. Visible pathology in male mice and decreased contractile strength relative to increased muscle weight suggest MSTN loss results in muscle impairment, which is dose-, sex-, and muscle-dependent. Muscle Nerve 43: 49-57, 2011

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