Lithium Chloride Regulates Connexin43 in Skeletal Myoblasts In Vitro: Possible Involvement in Wnt/-Catenin Signaling
Lithium Chloride Regulates Connexin43 in Skeletal Myoblasts In Vitro: Possible Involvement in Wnt/-Catenin Signaling
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DOI：
10.1080/15419060802198587
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发表时间：
2008-01-01
影响因子：
--
通讯作者：
Yu, B.
中科院分区：
文献类型：
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作者：
Du, W. J.;Li, J. K.;Yu, B.
缝隙连接蛋白43（connexin 43，Cx43）组成的缝隙连接通道对正常肌源性分化和骨骼肌再生至关重要。在这里，目的是研究氯化锂（LiCl）是否可以通过模拟原代成肌细胞中的Wnt/-catenin通路来调节Cx43表达和间隙连接通道功能。成肌细胞中Cx43 mRNA的表达上调5 mM氯化锂。用5和10 mM LiCl处理24 h导致的Cx43蛋白表达增强增加了成肌细胞中的缝隙连接偶联。然而，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慢性处理降低了Cx43蛋白表达。作者表明，LiCl通过糖原合成酶激酶-3（GSK-3）失活和效应蛋白-连环蛋白在细胞核中的积累来模拟活性经典Wnt/-连环蛋白信号传导。这些结果表明，氯化锂调节Cx43在骨骼肌成肌细胞在体外的表达部分通过Wnt/β-catenin依赖的途径。
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/-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/-catenin signaling by glycogen synthase kinase-3 (GSK-3) inactivation and accumulation of the effector protein -catenin into the nucleus. These results suggest that LiCl regulates Cx43 expression in skeletal myoblasts in vitro partly by a Wnt/-catenin-dependent pathway.