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Lithium Chloride Regulates Connexin43 in Skeletal Myoblasts In Vitro: Possible Involvement in Wnt/β-Catenin Signaling

机译:氯化锂体外调节骨骼肌成肌细胞中的connexin43:可能参与Wnt /β-Catenin信号传导

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摘要

Gap junction channels composed of connexin43 (Cx43) are essential for normal myogenic differentiation and skeletal muscle regeneration. Here, the aim was to study whether lithium chloride (LiCl) could regulate Cx43 expression and gap junction channel function by mimicking the Wnt/β-catenin pathway in primary myoblasts. Cx43 mRNA expression in myoblasts was up-regulated in response to 5 mM LiCl. The enhanced Cx43 protein expression resulting from treatment with 5 and 10 mM LiCl for 24 h increased gap-junctional coupling in myoblasts. However, no obvious changes were observed with 20 mM LiCl. Furthermore, chronic treatment with 10 mM LiCl decreased Cx43 protein expression compared with untreated cells. The authors showed that LiCl mimicked the active canonical Wnt/β-catenin signaling by glycogen synthase kinase-3β (GSK-3β) inactivation and accumulation of the effector protein β-catenin into the nucleus. These results suggest that LiCl regulates Cx43 expression in skeletal myoblasts in vitro partly by a Wnt/β-catenin-dependent pathway.
机译:由连接蛋白43(Cx43)组成的间隙连接通道对于正常的成肌分化和骨骼肌再生至关重要。在这里,目的是研究氯化锂(LiCl)是否可以通过模仿原代成肌细胞中的Wnt /β-catenin途径来调节Cx43表达和间隙连接通道功能。响应5 mM LiCl,成肌细胞中的Cx43 mRNA表达上调。用5和10 mM LiCl处理24小时后,增强的Cx43蛋白表达增强了成肌细胞中的缝隙连接偶联。但是,使用20 mM LiCl时未观察到明显变化。此外,与未处理的细胞相比,用10 mM LiCl进行的慢性治疗可降低Cx43蛋白的表达。作者表明,LiCl通过糖原合酶激酶3β(GSK-3β)失活并将效应蛋白β-catenin积聚到细胞核中,模仿了活跃的经典Wnt /β-catenin信号传导。这些结果表明,LiCl部分地通过Wnt /β-catenin依赖性途径调节骨骼肌成肌细胞中Cx43的表达。

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