arathyroid hormone and parathyroid hormonetype1- receptor accelerate myocyte differentiation

2014 Fiscal Year Final Research Report

• Project/Area Number: 24615005
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Regenerative medicine
• Research Institution: Kumamoto University
• Principal Investigator: KIMURA Shigemi 熊本大学, 大学院生命科学研究部, 准教授 (60284767)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: ES細胞 / DNAアレイ / 筋分化 / 筋芽細胞 / 副甲状腺ホルモンレセプター / 副甲状腺ホルモン / 筋ジストロフィー / 治療

Outline of Final Research Achievements

The ZHTc6-MyoD ES cell line expresses the myogenic transcriptional factor MyoD under the control of a tetracycline-inducible promoter. Following induction, most of the ZHTc6-MyoD cells differentiate to myotubes. However, a small fraction does not differentiate, instead forming colonies that retain the potential for myocyte differentiation. In our current study, we found that parathyroid hormone type 1 receptor (PTH1R) expression in colony-forming cells at 13 days after differentiation was higher than that in the undifferentiated ZHTc6-MyoD cells. We also found that PTH1R expression was required for myocyte differentiation, and that parathyroid hormone accelerated the differentiation. Our analysis of human and mouse skeletal muscle tissues showed that most cells expressing PTH1R also expressed Pax7 and CD34, which are biomarkers of satellite cells. Furthermore, we found that parathyroid hormone treatment significantly improved muscle weakness in dystrophin-deficient mdx mice.

Free Research Field

再生医療