Effects of heat shock protein and calcineurin in hypertrophied and atrophied skeletal muscles

在过去的两年里，我研究了热休克蛋白(HSP)和钙调神经磷酸酶(CaN)在肥大或萎缩的大鼠骨骼肌中的作用。克伦特罗注射大鼠后肢肌出现肥大，纤维表型由慢变快，慢比目鱼肌HSP72表达降低，CaN增加。通过切断其增效剂的肌腱，快速的足底肌功能超负荷(FO)导致肌纤维肥大和纤维表型由快向慢的转变。随着纤维大小的增加和纤维表型的减慢，HSP72在功能超负荷的足底中也表达上调。CaN的抑制剂环孢菌素A可抑制足底肌肉肥大和纤维表型的改变，表明CaN与纤维的大小和表型有关。另外，甲状腺激素(T3)对FO足底组织HSP72和CaN的表达水平有下调作用。

During passed two years, I investigated the effects of heat shock proteins (HSP) and calcineurin (CaN) in hypertrophied or atrophied rat skeletal muscles. In clenbuterol injected rat hindlimb muscles, which occurred hypertrophy and the shift of fiber phenotype from slow-to-fast, Hsp72 was decreased in the slow soleus muscle, where the CaN was increased. Functionally overload (FO) of fast plantaris muscle by cutting the tendons of its synergists induced muscle fiber hypertrophy and the shift of fiber phenotype from fast-to-slow. Hsp72 was also upregulated in functionally overloaded plantaris concomitantly with the increase in fiber size and slow fiber phenotype. Muscle hypertrophy and the shift of fiber phenotype observed in the FO plantaris was inhibited by the treatment of cyclosporin A, a inhibitor of CaN, indicating that the CaN was related to the fiber size and phenotype. In addition, thyroid hormone (T3) treatment to the FO plantaris downregulated to the expression level of the Hsp72 and CaN.