Robison Patrick, Sussan Thomas E, Chen Hegang, Biswal Shyam, Schneider Martin F, Hernández-Ochoa Erick O
Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, 108 N. Greene Street, Baltimore, Maryland, 21201, USA.
Department of Physiology, Pennsylvania Muscle Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Muscle Nerve. 2017 Aug;56(2):282-291. doi: 10.1002/mus.25466. Epub 2017 Feb 13.
Respiratory and locomotor skeletal muscle dysfunction are common findings in chronic obstructive pulmonary disease (COPD); however, the mechanisms that cause muscle impairment in COPD are unclear. Because Ca signaling in excitation-contraction (E-C) coupling is important for muscle activity, we hypothesized that Ca dysregulation could contribute to muscle dysfunction in COPD.
Intercostal and flexor digitorum brevis muscles from control and cigarette smoke-exposed mice were investigated. We used single cell Ca imaging and Western blot assays to assess Ca signals and E-C coupling proteins.
We found impaired Ca signals in muscle fibers from both muscle types, without significant changes in releasable Ca or in the expression levels of E-C coupling proteins.
Ca dysregulation may contribute or accompany respiratory and locomotor muscle dysfunction in COPD. These findings are of significance to the understanding of the pathophysiological course of COPD in respiratory and locomotor muscles. Muscle Nerve 56: 282-291, 2017.
呼吸和运动骨骼肌功能障碍是慢性阻塞性肺疾病(COPD)的常见表现;然而,COPD中导致肌肉损伤的机制尚不清楚。由于兴奋-收缩(E-C)偶联中的钙信号对肌肉活动很重要,我们推测钙调节异常可能导致COPD中的肌肉功能障碍。
研究了来自对照小鼠和暴露于香烟烟雾的小鼠的肋间肌和趾短屈肌。我们使用单细胞钙成像和蛋白质印迹分析来评估钙信号和E-C偶联蛋白。
我们发现两种肌肉类型的肌纤维中钙信号均受损,可释放钙或E-C偶联蛋白的表达水平无显著变化。
钙调节异常可能导致或伴随COPD中的呼吸和运动肌肉功能障碍。这些发现对于理解COPD在呼吸和运动肌肉中的病理生理过程具有重要意义。《肌肉与神经》56: 282 - 291, 2017年。