Study on Mechano-Sensing Channel in muscular dystrophic dog

已有多项研究报道了肌营养不良症骨骼肌和心肌细胞内钙离子浓度升高。细胞内钙离子浓度的慢性升高可激活钙依赖的细胞信号转导通路，导致细胞坏死。然而，在肌营养不良症中控制钙离子内流的细胞机制仍不清楚。Trp通道形成了一大类阳离子通道，它们可能在不同的过程中起到四聚体的作用，如感觉信号，其中大多数对钙离子是通透的，也有一些对镁离子也是通透的。为了探讨Trp家族与肌肉退行性变的关系，我们分析了Trp通道在Duchenne肌营养不良犬模型骨骼肌和心肌中的表达。

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.