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Variation in ACE activity affects myogenic differentiation in C2C12 cells.

机译:ACE活性的变化会影响C2C12细胞的成肌分化。

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摘要

Variation in ACE activity is related to affect the skeletal muscle function. To elucidate the mechanism by which ACE affects skeletal muscle function, we examined the effects of loss and gain of ACE activity on myogenic differentiation in C2C12 myoblasts. The treatment of captopril, an ACE inhibitor, in differentiating cells significantly induced the up-regulation of myosin heavy chain, and the hypertrophic myotubes. In addition, an AT2 antagonist PD123319, not AT1 antagonist losartan, induced the up-regulation of myosin heavy chain. On the other hand, overexpression of ACE induced the down-regulation of myosin heavy chain. These results suggest that ACE negatively regulate the myogenesis through the mechanism at least in part via production of angiotensin II followed by its binding to AT2 receptor.
机译:ACE活性的变化与影响骨骼肌功能有关。为了阐明ACE影响骨骼肌功能的机制,我们研究了ACE活性丧失和获得对C2C12成肌细胞分化的影响。在分化细胞中对ACE抑制剂卡托普利的治疗显着诱导了肌球蛋白重链和肥大性肌管的上调。另外,AT2拮抗剂PD123319而非AT1拮抗剂氯沙坦诱导肌球蛋白重链的上调。另一方面,ACE的过度表达引起肌球蛋白重链的下调。这些结果表明,ACE至少部分地通过血管紧张素II的产生并随后与AT2受体结合而通过该机制负调控肌发生。

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