Genetic Models in Applied Physiology. Merosin deficiency leads to alterations in passive and active skeletal muscle mechanics.
Genetic Models in Applied Physiology. Merosin deficiency leads to alterations in passive and active skeletal muscle mechanics.
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应用生理学中的遗传模型。
DOI：
10.1152/japplphysiol.01078.2002
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发表时间：
2003
期刊：
影响因子：
--
通讯作者：
Boriek,AladinM
中科院分区：
文献类型：
--
作者：
Jannapureddy,SunealR;Patel,NishaD;Hwang,Willy;Boriek,AladinM
细胞外元素对骨骼肌力学性能的影响尚不清楚。Merosin是一种重要的细胞外基质蛋白，在肌膜和胶原之间形成机械连接。因此，Merosin可能在肌肉纤维和胶原蛋白之间的力传递中发挥作用。我们假设，缺乏Merosin可能会改变骨骼肌中被动肌肉的僵硬、粘弹性和收缩肌力。我们使用了一种Merosin缺乏的小鼠模型-dy/dy小鼠，来检查被动和主动肌肉力学的变化。麻醉小鼠，切除横隔肌或股二头肌后肢肌，用体外双轴力学测试仪测定被动长度-张力关系、应力-松弛曲线或等长收缩特性。与对照组相比，突变小鼠的肌纤维方向和横向纤维方向的延伸性较小。与对照组相比，Merosin缺乏的横隔膜的松弛弹性模数较小。有趣的是，突变小鼠肌肉中的最大肌肉强直性应力在单轴加载时被抑制，但在双轴加载时不被抑制。然而，横向被动拉伸的存在增加了突变小鼠和正常小鼠的最大收缩应力。我们的数据表明，Merosin有助于肌肉的被动僵硬、粘弹性和伸缩性，力通过Merosin在相邻肌纤维之间传递的机制可能是剪切的。
The role of extracellular elements on the mechanical properties of skeletal muscles is unknown. Merosin is an essential extracellular matrix protein that forms a mechanical junction between the sarcolemma and collagen. Therefore, it is possible that merosin plays a role in force transmission between muscle fibers and collagen. We hypothesized that deficiency in merosin may alter passive muscle stiffness, viscoelastic properties, and contractile muscle force in skeletal muscles. We used thedy/dymouse, a merosin-deficient mouse model, to examine changes in passive and active muscle mechanics. After mice were anesthetized and the diaphragm or the biceps femoris hindlimb muscle was excised, passive length-tension relationships, stress-relaxation curves, or isometric contractile properties were determined with an in vitro biaxial mechanical testing apparatus. Compared with controls, extensibility was smaller in the muscle fiber direction and the transverse fiber direction of the mutant mice. The relaxed elastic modulus was smaller in merosin-deficient diaphragms compared with controls. Interestingly, maximal muscle tetanic stress was depressed in muscles from the mutant mice during uniaxial loading but not during biaxial loading. However, presence of transverse passive stretch increases maximal contractile stress in both the mutant and normal mice. Our data suggest that merosin contributes to muscle passive stiffness, viscoelasticity, and contractility and that the mechanism by which force is transmitted between adjacent myofibers via merosin possibly in shear.