Delbono Osvaldo, Xia Jinyu, Treves Susan, Wang Zhong-Min, Jimenez-Moreno Ramon, Payne Anthony M, Messi María Laura, Briguet Alexandre, Schaerer Florian, Nishi Miyuki, Takeshima Hiroshi, Zorzato Francesco
Departments of Anaesthesia and Research, Basel University Hospital, Hebelstrasse 20, 4031 Basel, Switzerland.
Proc Natl Acad Sci U S A. 2007 Dec 11;104(50):20108-13. doi: 10.1073/pnas.0707389104. Epub 2007 Dec 5.
Skeletal muscle constitutes approximately 40% of the human body mass, and alterations in muscle mass and strength may result in physical disability. Therefore, the elucidation of the factors responsible for muscle force development is of paramount importance. Excitation-contraction coupling (ECC) is a process during which the skeletal muscle surface membrane is depolarized, causing a transient release of calcium from the sarcoplasmic reticulum that activates the contractile proteins. The ECC machinery is complex, and the functional role of many of its protein components remains elusive. This study demonstrates that deletion of the gene encoding the sarcoplasmic reticulum protein JP45 results in decreased muscle strength in young mice. Specifically, this loss of muscle strength in JP45 knockout mice is caused by decreased functional expression of the voltage-dependent Ca(2+) channel Ca(v)1.1, which is the molecule that couples membrane depolarization and calcium release from the sarcoplasmic reticulum. These results point to JP45 as one of the molecules involved in the development or maintenance of skeletal muscle strength.
骨骼肌约占人体体重的40%，肌肉质量和力量的改变可能导致身体残疾。因此，阐明负责肌肉力量发展的因素至关重要。兴奋-收缩偶联（ECC）是一个过程，在此过程中骨骼肌表面膜去极化，导致肌浆网中钙的瞬时释放，从而激活收缩蛋白。ECC机制复杂，其许多蛋白质成分的功能作用仍不清楚。本研究表明，编码肌浆网蛋白JP45的基因缺失会导致幼鼠肌肉力量下降。具体而言，JP45基因敲除小鼠肌肉力量的丧失是由电压依赖性Ca(2+)通道Ca(v)1.1功能表达降低引起的，Ca(v)1.1是将膜去极化与肌浆网钙释放相偶联的分子。这些结果表明JP45是参与骨骼肌力量发展或维持的分子之一。
