Electroacupuncture suppresses myostatin gene expression: cell proliferative reaction in mouse skeletal muscle
Author(s) -
Yutaka Takaoka,
Mika Ohta,
Akihiko Ito,
Kunihiko Takamatsu,
Aki Sugano,
Kotaro Funakoshi,
N. Takaoka,
Nobuko Sato,
Hiroshi Yokozaki,
Naoki Arizono,
Shuji Goto,
Eiichi Maeda
Publication year - 2007
Publication title -
physiological genomics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.078
H-Index - 112
eISSN - 1531-2267
pISSN - 1094-8341
DOI - 10.1152/physiolgenomics.00057.2006
Subject(s) - myostatin , skeletal muscle , biology , cell growth , gene expression , proliferating cell nuclear antigen , cell , gene , medicine , endocrinology , microbiology and biotechnology , genetics
Complementary and alternative medicine (CAM) may provide patients with an alternative to traditional medicine, but an assessment of its efficacy is required. One CAM method, electroacupuncture (EA) treatment, is a maneuver that utilizes stimulation of acupuncture needles with a low-frequency microcurrent. To study the effect of short-term EA, we evaluated the differential expression of genes induced by EA in mouse skeletal muscle for up to 24 h. We then used RT-PCR to confirm the expression patterns of six differentially expressed genes. Bioinformatics analysis of their transcription control regions showed that EA-inducible genes have numerous common binding motifs that are related to cell differentiation, cell proliferation, muscle repair, and hyperplasia. These results suggested that EA treatment may induce cell proliferation in skeletal muscle. To verify this possibility, we used EA to stimulate mouse skeletal muscle daily for up to 1 mo and examined the long-term effects. Immunohistochemical analysis showed that nuclei of muscle cells treated with EA for 1 mo, especially nuclei of satellite cells, reacted with anti-human PCNA. Also, expression of the gene encoding myostatin, which is a growth repressor in muscle satellite cells, was suppressed by daily EA treatment for 1 wk; EA treatment for 1 mo resulted in more marked suppression of the gene. These molecular findings constitute strong evidence that EA treatment suppresses myostatin expression, which leads to a satellite cell-related proliferative reaction and repair in skeletal muscle.
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