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首页> 外文期刊>American Journal of Physiology >In vivo expression patterns of MyoD, p21, and Rb proteins in myonuclei and satellite cells of denervated rat skeletal muscle.
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In vivo expression patterns of MyoD, p21, and Rb proteins in myonuclei and satellite cells of denervated rat skeletal muscle.

机译：MyoD，p21和Rb蛋白在失神经的大鼠骨骼肌的肌核和卫星细胞中的体内表达模式。

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摘要

MyoD, a myogenic regulatory factor, is rapidly expressed in adult skeletal muscles in response to denervation. However, the function(s) of MyoD expressed in denervated muscle has not been adequately elucidated. In vitro, it directly transactivates cyclin-dependent kinase inhibitor p21 (p21) and retinoblastoma protein (Rb), a downstream target of p21. These factors then act to regulate cell cycle withdrawal and antiapoptotic cell death. Using immunohistochemical approaches, we characterized cell types expressing MyoD, p21, and Rb and the relationship among these factors in the myonucleus of denervated muscles. In addition, we quantitatively examined the time course changes and expression patterns among distinct myofiber types of MyoD, p21, and Rb during denervation. Denervation induced MyoD expression in myonuclei and satellite cell nuclei, whereas p21 and Rb were found only in myonuclei. Furthermore, coexpression of MyoD, p21, and Rb was induced in the myonucleus, and quantitative analysis of these factors determined that there was no difference among the three myofiber types. These observations suggest that MyoD may function in myonuclei in response to denervation to protect against denervation-induced apoptosis via perhaps the activation of p21 and Rb, and function of MyoD expressed in satellite cell nuclei may be negatively regulated. The present study provides a molecular basis to further understand the function of MyoD expressed in the myonuclei and satellite cell nuclei of denervated skeletal muscle.
机译：MyoD是一种成肌调节因子，响应于神经支配在成年骨骼肌中快速表达。然而，尚未充分阐明在失神经的肌肉中表达的MyoD的功能。在体外，它直接激活细胞周期蛋白依赖性激酶抑制剂p21（p21）和成视网膜细胞瘤蛋白（Rb）（p21的下游靶标）。这些因子然后起作用以调节细胞周期停药和抗凋亡细胞死亡。使用免疫组织化学方法，我们表征了表达神经肌肉，肌腱，p21和Rb和这些因素之间的关系的细胞类型。此外，我们定量检查了去神经过程中MyoD，p21和Rb不同肌纤维类型之间的时程变化和表达模式。去神经作用诱导了MyoD在肌核和卫星细胞核中的表达，而p21和Rb仅在肌核中发现。此外，在肌核中诱导了MyoD，p21和Rb的共表达，并且对这些因素的定量分析确定这三种肌纤维之间没有差异。这些观察结果表明，MyoD可能在神经支配反应中发挥作用，可能通过p21和Rb的激活来防止神经支配诱导的凋亡，卫星细胞核中表达的MyoD的功能可能受到负调控。本研究提供了分子基础，以进一步了解失神经化的骨骼肌的肌核和卫星细胞核中表达的MyoD的功能。

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