肌肉生长抑制素缺失小鼠后肢骨骼肌功能。
Hindlimb skeletal muscle function in myostatin-deficient mice.
机构信息
Department of Veterinary Pathobiology, University of Missouri, Columbia, Missouri, USA.
出版信息
Muscle Nerve. 2011 Jan;43(1):49-57. doi: 10.1002/mus.21796.
Abstract
Absence of functional myostatin (MSTN) during fetal development results in adult skeletal muscle hypertrophy and hyperplasia. To more fully characterize MSTN loss in hindlimb 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.
摘要
在胎儿发育过程中缺乏功能性肌肉生长抑制素（MSTN）会导致成年骨骼肌肥大和增生。为了更全面地描述后肢肌肉中 MSTN 的缺失，对雄性和雌性 MSTN 缺失（Mstn(-/-)）、杂合子（Mstn(+/-)）和野生型（Mstn(+/+)）小鼠的比目鱼肌、跖肌、腓肠肌、胫骨前肌和四头肌的形态和收缩功能进行了研究。Mstn(-/-)小鼠的肌肉重量大于 Mstn(+/+)和 Mstn(+/-)小鼠。雌性 Mstn(-/-)比目鱼肌和腓肠肌以及雄性 Mstn(-/-)小鼠的四头肌的肌纤维横截面积（CSA）增加；Mstn(-/-)小鼠的最大强直力与增加的肌肉重量或 CSA 不成正比。雄性 Mstn(-/-)肌肉表现出中度退化。雄性小鼠可见的病理变化和相对于增加的肌肉重量收缩力的下降表明 MSTN 的缺失导致肌肉损伤，这取决于剂量、性别和肌肉。
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