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首页> 外文期刊>American Journal of Physiology >Dexamethasone stimulates store-operated calcium entry and protein degradation in cultured L6 myotubes through a phospholipase A(2)-dependent mechanism.
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Dexamethasone stimulates store-operated calcium entry and protein degradation in cultured L6 myotubes through a phospholipase A(2)-dependent mechanism.

机译：地塞米松通过磷脂酶A（2）依赖性机制刺激培养的L6肌管中的存储操作钙进入和蛋白质降解。

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摘要

Muscle wasting in various catabolic conditions is at least in part regulated by glucocorticoids. Increased calcium levels have been reported in atrophying muscle. Mechanisms regulating calcium homeostasis in muscle wasting, in particular the role of glucocorticoids, are poorly understood. Here we tested the hypothesis that glucocorticoids increase intracellular calcium concentrations in skeletal muscle and stimulate store-operated calcium entry (SOCE) and that these effects of glucocorticoids may at least in part be responsible for glucocorticoid-induced protein degradation. Treatment of cultured myotubes with dexamethasone, a frequently used in vitro model of muscle wasting, resulted in increased intracellular calcium concentrations determined by fura-2 AM fluorescence measurements. When SOCE was measured by using calcium "add-back" to muscle cells after depletion of intracellular calcium stores, results showed that SOCE was increased 15-25% by dexamethasone and that this response to dexamethasone was inhibited by the store-operated calcium channel blocker BTP2. Dexamethasone treatment stimulated the activity of calcium-independent phospholipase A(2) (iPLA(2)), and dexamethasone-induced increase in SOCE was reduced by the iPLA(2) inhibitor bromoenol lactone (BEL). In additional experiments, treatment of myotubes with the store-operated calcium channel inhibitor gadolinium ion or BEL reduced dexamethasone-induced increase in protein degradation. Taken together, the results suggest that glucocorticoids increase calcium concentrations in myocytes and stimulate iPLA(2)-dependent SOCE and that glucocorticoid-induced muscle protein degradation may at least in part be regulated by increased iPLA(2) activity, SOCE, and cellular calcium levels.
机译：在各种分解代谢条件下的肌肉消耗至少部分受糖皮质激素调节。据报道萎缩肌肉中钙水平升高。对肌肉消瘦中钙动态平衡的调节机制，尤其是糖皮质激素的作用了解甚少。在这里，我们测试了以下假设：糖皮质激素会增加骨骼肌中细胞内钙的浓度，并刺激储存钙离子进入（SOCE），并且糖皮质激素的这些作用可能至少部分负责糖皮质激素诱导的蛋白质降解。用地塞米松治疗培养的肌管，地塞米松是肌肉消瘦的一种常用体外模型，导致通过呋喃2 AM荧光测量确定的细胞内钙浓度升高。当细胞内钙储存耗尽后，通过在肌肉细胞中使用钙“添加”钙来测量SOCE时，结果显示地塞米松可使SOCE升高15-25％，而对地塞米松的这种反应受到储藏操作的钙通道阻滞剂的抑制BTP2。地塞米松治疗刺激了钙独立磷脂酶A（2）（iPLA（2））的活性，地塞米松诱导的SOCE的增加被iPLA（2）抑制剂溴烯醇内酯（BEL）减少。在其他实验中，用储库操作的钙通道抑制剂g离子或BEL处理肌管可减少地塞米松诱导的蛋白质降解增加。两者合计，结果表明糖皮质激素增加肌细胞中的钙浓度并刺激iPLA（2）依赖的SOCE，糖皮质激素诱导的肌肉蛋白降解可能至少部分受iPLA（2）活性，SOCE和细胞钙增加的调节水平。

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