School of Biological Sciences, University of Reading, Reading, UK.
J Anat. 2012 Jun;220(6):603-11. doi: 10.1111/j.1469-7580.2012.01503.x. Epub 2012 Mar 30.
Myostatin is a potent inhibitor of muscle development. Genetic deletion of myostatin in mice results in muscle mass increase, with muscles often weighing three times their normal values. Contracting muscle transfers tension to skeletal elements through an elaborate connective tissue network. Therefore, the connective tissue of skeletal muscle is an integral component of the contractile apparatus. Here we examine the connective tissue architecture in myostatin null muscle. We show that the hypertrophic muscle has decreased connective tissue content compared with wild-type muscle. Secondly, we show that the hypertrophic muscle fails to show the normal increase in muscle connective tissue content during ageing. Therefore, genetic deletion of myostatin results in an increase in contractile elements but a decrease in connective tissue content. We propose a model based on the contractile profile of muscle fibres that reconciles this apparent incompatible tissue composition phenotype.
肌肉生长抑制素是一种有效的肌肉发育抑制剂。在小鼠中基因删除肌肉生长抑制素会导致肌肉质量增加,肌肉重量通常是正常的三倍。收缩肌肉通过一个复杂的结缔组织网络将张力传递到骨骼元素。因此,骨骼肌的结缔组织是收缩装置的一个组成部分。在这里,我们检查了肌肉生长抑制素缺失肌肉中的结缔组织结构。我们发现,与野生型肌肉相比,肥大肌肉的结缔组织含量减少。其次,我们发现,在衰老过程中,肥大肌肉没有表现出正常的肌肉结缔组织含量增加。因此,肌肉生长抑制素的基因缺失导致收缩成分增加,但结缔组织含量减少。我们提出了一个基于肌肉纤维收缩特性的模型,该模型解释了这种明显不协调的组织组成表型。