期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 18, 期 1, 页码 -出版社
MDPI
DOI: 10.3390/ijms18010115
关键词
myoblast; transthyretin; proliferation; differentiation
资金
- Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Education [2016R1C1B1011478]
- National Research Foundation of Korea (NRF) - Korean government (MSIP) [2014R1A2A2A01006324]
- National Research Foundation of Korea [2014R1A2A2A01006324, 2016R1C1B1011478] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Irregularities in the cellular uptake of thyroid hormones significantly affect muscle development and regeneration. Herein, we report indispensable role of transthyretin (TTR) in maintaining cellular thyroxine level. TTR was found to enhance recruitment of muscle satellite cells to the site of injury, thereby regulating muscle regeneration. Fluorescence-activated cell sorting (FACS) and immunofluorescence analysis of TTRwt (TTR wild type) and TTRkd (TTR knock-down) cells revealed that TTR controlled cell cycle progression by affecting the expression of Cyclin A2. Deiodinase 2 (D2) mediated increases in triiodothyronine levels were found to regulate the expression of myogenic marker, myogenin (MYOG). Moreover, use of a coumarin derivative (CD) revealed a significant reduction in cellular thyroxine, thereby indicating that TTR play a role in the transport of thyroxine. Taken together, these findings suggest that TTR mediated transport of thyroxine represents a survival mechanism necessary for the myogenic program. The results of this study will be highly useful to the strategic development of novel therapeutics to combat muscular dystrophies.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据