Femoral morphology and cross-sectional geometry of adult myostatin-deficient mice
Femoral morphology and cross-sectional geometry of adult myostatin-deficient mice
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DOI：
10.1016/s8756-3282(00)00339-2
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发表时间：
2000-09-01
期刊：
影响因子：
4.1
通讯作者：
Hudson, J
中科院分区：
文献类型：
--
作者：
Hamrick, MW;McPherron, AC;Hudson, J
GDF-8又称myostatin，是脊椎动物骨骼肌中表达的分泌生长和分化因子超家族中的一员。肌肉生长抑制素是骨骼肌生长的负调节因子，与正常小鼠相比，肌肉抑制素基因缺失的小鼠的肌肉质量增加了一倍。我们研究了成年myostatin缺失小鼠的股骨形态，以评估肌肉纤维肥大和增殖对骨骼形状和横断面几何形状的影响，将年龄和体重匹配的纯合myostatin序列缺失的成年小鼠的股骨与野生型对照组(每组8只)进行比较，结果表明，与以前的研究一样，myostatin缺失小鼠的后肢肌肉质量大约是对照组的两倍。肌肉抑制素缺陷小鼠的第三大转子明显大于对照组，而对照组和实验组小鼠的股骨中轴在皮质面积、弯曲转动惯量和极转动惯量方面没有显著差异。我们的发现表明，与对照组相比，肌肉抑制素缺陷小鼠肌肉质量的增加主要影响肌肉插入部位，但不会在骨干中诱导额外的皮质骨沉积。因此，我们得出结论，肌肉抑制素缺乏受试者的第三大转子扩张是肌腱和Sharpey纤维扩张与肌肉生长相关的结果，而不是由于机械应力水平的增加而导致的皮质骨沉积。(C)2000，爱思唯尔科学公司。保留所有权利。
GDF-8, also known as myostatin, is a member of the transforming growth factor-beta (TGF-beta) superfamily of secreted growth and differentiation factors that is expressed in vertebrate skeletal muscle. Myostatin functions as a negative regulator of skeletal muscle growth and myostatin null mice show a doubling of muscle mass compared with normal mice. We examined femoral morphology of adult myostatin-deficient mice to assess the effects of muscle fiber hypertrophy and hyperplasia on bone shape and cross-sectional geometry, Femora of age- and weight-matched adult mice homozygous for the disrupted myostatin sequence were compared with those of wild-type controls (n = 8 per group), Results show that, as was the case in previous studies, myostatin null mice have hindlimb muscle masses that are approximately double those of controls. Myostatin-deficient mice exhibit third trochanters that are significantly larger than those of controls, whereas the femoral midshafts of the control and experimental mice no not differ significantly from one another in cortical area, bending moment of inertia, and polar moment of inertia. Our findings indicate that the increased muscle mass of myostatin-deficient mice primarily affects sites of muscle insertion, but does not induce additional cortical bone deposition in the diaphysis relative to controls. We therefore conclude that the expanded third trochanters of myostatin-deficient subjects result from tendon and Sharpey fiber expansion associated with muscle growth rather than cortical bone deposition in response to increased levels of mechanical stress. (C) 2000 by Elsevier Science Inc. All rights reserved.