論文

査読有り 国際誌
2020年2月27日

Expression Levels of Long Non-Coding RNAs Change in Models of Altered Muscle Activity and Muscle Mass.

International journal of molecular sciences
  • Keisuke Hitachi
  • ,
  • Masashi Nakatani
  • ,
  • Shiori Funasaki
  • ,
  • Ikumi Hijikata
  • ,
  • Mizuki Maekawa
  • ,
  • Masahiko Honda
  • ,
  • Kunihiro Tsuchida

21
5
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.3390/ijms21051628

Skeletal muscle is a highly plastic organ that is necessary for homeostasis and health of the human body. The size of skeletal muscle changes in response to intrinsic and extrinsic stimuli. Although protein-coding RNAs including myostatin, NF-κβ, and insulin-like growth factor-1 (IGF-1), have pivotal roles in determining the skeletal muscle mass, the role of long non-coding RNAs (lncRNAs) in the regulation of skeletal muscle mass remains to be elucidated. Here, we performed expression profiling of nine skeletal muscle differentiation-related lncRNAs (DRR, DUM1, linc-MD1, linc-YY1, LncMyod, Neat1, Myoparr, Malat1, and SRA) and three genomic imprinting-related lncRNAs (Gtl2, H19, and IG-DMR) in mouse skeletal muscle. The expression levels of these lncRNAs were examined by quantitative RT-PCR in six skeletal muscle atrophy models (denervation, casting, tail suspension, dexamethasone-administration, cancer cachexia, and fasting) and two skeletal muscle hypertrophy models (mechanical overload and deficiency of the myostatin gene). Cluster analyses of these lncRNA expression levels were successfully used to categorize the muscle atrophy models into two sub-groups. In addition, the expression of Gtl2, IG-DMR, and DUM1 was altered along with changes in the skeletal muscle size. The overview of the expression levels of lncRNAs in multiple muscle atrophy and hypertrophy models provides a novel insight into the role of lncRNAs in determining the skeletal muscle mass.

リンク情報
DOI
https://doi.org/10.3390/ijms21051628
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/32120896
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7084395
ID情報
  • DOI : 10.3390/ijms21051628
  • PubMed ID : 32120896
  • PubMed Central 記事ID : PMC7084395

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