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1 Graduate School of Sport and Exercise Science, Osaka University of Health and Sport Sciences, Osaka, Japan
2 Graduate School of Sport and Health Science, Osaka University of Health and Sport Sciences, Osaka, Japan
* To whom correspondence should be addressed. E-mail: 202d01{at}ouhs.ac.jp.
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 down-stream target of p21. These factors then act to regulate cell cycle withdrawal and anti-apoptotic cell death. Using immunohistochemical approaches, we characterized cell types expressing MyoD, p21 and Rb and relationship among these factors in 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, while p21 and Rb were found only in myonuclei. Furthermore, co-expression 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 function of MyoD expressed in the myonuclei and satellite cell nuclei of denervated skeletal muscle.
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