Study on Mechano-Sensing Channel in muscular dystrophic dog

许多研究报道了肌营养不良的骨骼肌和心肌的细胞质Ca2+浓度升高。细胞内Ca2+浓度的长期升高可激活Ca2+依赖性细胞信号级联，诱导细胞坏死。然而，肌肉萎缩症中控制Ca2+内流的细胞机制仍然未知。TRP通道形成了一个大家族的阳离子通道，可能在各种过程中作为四聚体起作用，例如感觉信号，其中大多数可渗透Ca2+，有些也可渗透Mg2+。为了确定TRP家族与肌肉退行性变的关系，我们分析了犬杜氏肌营养不良模型骨骼肌和心肌中TRP通道的表达。

A number of studies have reported the elevation of the cytosolic Ca2+ concentration in skeletal and cardiac muscles of muscular dystrophy. Chronic elevation of the cytosolic Ca2+ concentration could activate Ca2+-dependent cell signaling cascade and induce cell necrosis. The cellular mechanism for controlling Ca2+ influx in muscular dystrophy, however, is still unknown. The TRP channels form a large family of cation channels that likely function as tetramers in various processes, such as sensory signaling, most of which are permeable for Ca2+, and some also for Mg2+. To determine the relationship between TRP family and muscle degeneration, we analyzed the expression of TRP channel in skeletal and cardiac muscle of Canine models of Duchenne muscular dystrophy.