4.5 Article

MicroRNA-1 and microRNA-133a expression are decreased during skeletal muscle hypertrophy

Journal

JOURNAL OF APPLIED PHYSIOLOGY
Volume 102, Issue 1, Pages 306-313

Publisher

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/japplphysiol.00932.2006

Keywords

gene regulation; skeletal muscle hypertrophy

Funding

  1. NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR045617] Funding Source: NIH RePORTER
  2. NIAMS NIH HHS [AR-45617] Funding Source: Medline

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MicroRNAs ( miRNAs) are a class of highly conserved, noncoding RNAs involved in posttranscriptional gene regulation. A small number of muscle-specific miRNAs have been identified and shown to have a role in myoblast proliferation and differentiation as well as embryonic muscle growth. The primary objective of the present study was to determine the expression level of the muscle-specific miRNAs in the soleus and plantaris muscles and whether their expression in the plantaris was altered in response to functional overload. Of the miRNAs examined, only miRNA-206 was differentially expressed between soleus and plantaris muscles, as reflected by the sevenfold higher expression in the soleus for both the primary miRNA ( pri-miRNA) and mature miRNA ( miR). Following 7 days of functional overload, transcript levels for both pri-miRNA-1-2 and pri-miRNA-133a-2 increased by similar to 2-fold, whereas pri-miRNA-206 levels were elevated 18.3-fold. In contrast, expression of miR-1 and miR-133a were downregulated by similar to 50% following overload. The discrepancy between pri-miRNA and miR expression following overload was not explained by a change in the expression of components of the miRNA biogenesis pathway, since Drosha and Exportin-5 transcript levels were significantly increased by 50% in response to functional overload, whereas Dicer expression remained unchanged. These results are the first to report alterations in expression of muscle-specific miRNAs in adult skeletal muscle and suggest miRNAs may have a role in the adaptation to functional overload.

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