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缝隙连接蛋白 39 缺乏小鼠表现出骨骼肌的成肌作用和再生加速。

Connexin39 deficient mice display accelerated myogenesis and regeneration of skeletal muscle.

机构信息

Institute of Genetics, University of Bonn, D-53117 Bonn, Germany.

出版信息

Exp Cell Res. 2011 May 1;317(8):1169-78. doi: 10.1016/j.yexcr.2011.01.017. Epub 2011 Jan 24.

Abstract

During muscle development and regeneration of skeletal muscle in mice connexin43 (Cx43) and connexin39 (Cx39) are specifically expressed: Cx43 in satellite cells and myoblasts, whereas Cx39 is exclusively expressed in myogenin-positive cells. We generated Cx39 deficient mice by replacing the coding region of the Gjd4 gene by DNA coding for the enhanced green fluorescent protein eGFP. Adult Cx39 deficient mice exhibit no obvious phenotypic alterations of skeletal muscle compared to wild type mice in the resting state. However, myogenesis in Cx39 deficient embryos is accelerated as indicated by increased myogenin expression on ED13.5 and ED16.5 and increased expression of Cx43 in developing skeletal muscle. In addition, the regeneration process of skeletal muscle in Cx39 deficient mice is accelerated as shown by a 2day earlier onset of MyoD and myogenin expression, relative to wild type littermates. Interestingly, Cx43 expression was also upregulated in Cx39 deficient mice during regeneration of skeletal muscle. We hypothesize that Cx43 may compensate for the loss of Cx39 during myogenesis and regeneration.

摘要

在小鼠的肌肉发育和骨骼肌再生过程中,连接蛋白 43(Cx43)和连接蛋白 39(Cx39)特异性表达:Cx43 在卫星细胞和成肌细胞中表达,而 Cx39 仅在肌生成素阳性细胞中表达。我们通过用编码增强型绿色荧光蛋白 eGFP 的 DNA 替换 Gjd4 基因的编码区,生成了 Cx39 缺陷型小鼠。与野生型小鼠相比,成年 Cx39 缺陷型小鼠在静息状态下骨骼肌的表型没有明显改变。然而,Cx39 缺陷型胚胎中的成肌作用加速,表现为 ED13.5 和 ED16.5 时肌生成素表达增加,以及发育中的骨骼肌中 Cx43 的表达增加。此外,Cx39 缺陷型小鼠骨骼肌的再生过程也加速,表现为 MyoD 和肌生成素的表达比野生型同窝仔鼠早 2 天开始。有趣的是,Cx43 在 Cx39 缺陷型小鼠骨骼肌再生过程中的表达也上调。我们假设 Cx43 可能在成肌和再生过程中补偿 Cx39 的缺失。

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