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首页> 外文期刊>Cell biology international. >The mammalian target of rapamycin signaling pathway regulates myocyte enhancer factor-2C phosphorylation levels through integrin-linked kinase in goat skeletal muscle satellite cells
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The mammalian target of rapamycin signaling pathway regulates myocyte enhancer factor-2C phosphorylation levels through integrin-linked kinase in goat skeletal muscle satellite cells

机译：雷帕霉素信号转导途径的哺乳动物靶标通过整合素连接的激酶调节山羊骨骼肌卫星细胞中的心肌细胞增强因子2C磷酸化水平

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摘要

Mammalian target of rapamycin (mTOR) signaling pathway plays a key role in muscle development and is involved in multiple intracellular signaling pathways. Myocyte enhancer factor-2 (MEF2) regulates muscle cell proliferation and differentiation. However, how the mTOR signaling pathway regulates MEF2 activity remains unclear. We isolated goat skeletal muscle satellite cells (gSSCs) as model cells to explore mTOR signaling pathway regulation of MEF2C. We inhibited mTOR activity in gSSCs with PP242 and found that MEF2C phosphorylation was decreased and that muscle creatine kinase (MCK) expression was suppressed. Subsequently, we detected integrin-linked kinase (ILK) using MEF2C coimmunoprecipitation; ILK and MEF2C were colocalized in the gSSCs. We found that inhibiting mTOR activity increased ILK phosphorylation levels and that inhibiting ILK activity with Cpd 22 and knocking down ILK with small interfering RNA increased MEF2C phosphorylation and MCK expression. In the presence of Cpd 22, mTOR activity inhibition did not affect MEF2C phosphorylation. Moreover, ILK dephosphorylated MEF2C in vitro. These results suggest that the mTOR signaling pathway regulates MEF2C positively and regulates ILK negatively and that ILK regulates MEF2C negatively. It appears that the mTOR signaling pathway regulates MEF2C through ILK, further regulating the expression of muscle-related genes in gSSCs.
机译：雷帕霉素（mTOR）信号转导通路的哺乳动物目标在肌肉发育中起关键作用，并参与多个细胞内信号转导通路。心肌细胞增强因子2（MEF2）调节肌肉细胞的增殖和分化。然而，尚不清楚mTOR信号通路如何调节MEF2活性。我们分离了山羊骨骼肌卫星细胞（gSSCs）作为模型细胞，以探索MEF2C的mTOR信号通路调控。我们用PP242抑制了gSSC中的mTOR活性，发现MEF2C的磷酸化降低，肌肉肌酸激酶（MCK）的表达受到抑制。随后，我们使用MEF2C免疫沉淀法检测了整合素连接的激酶（ILK）; ILK和MEF2C在gSSC中共定位。我们发现抑制mTOR活性会增加ILK的磷酸化水平，而用Cpd 22抑制ILK活性并用小的干扰RNA抑制ILK会增加MEF2C磷酸化和MCK表达。在Cpd 22存在下，mTOR活性抑制不影响MEF2C磷酸化。此外，ILK在体外使MEF2C脱磷酸。这些结果表明，mTOR信号通路正向调节MEF2C而负向调节ILK，而ILK负向调节MEF2C。看来，mTOR信号通路通过ILK调节MEF2C，从而进一步调节gSSC中肌肉相关基因的表达。

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