title: Electroacupuncture suppresses myostatin gene expression: cell proliferative reaction in mouse skeletal muscle.
abstract: 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.
authors.affiliation: Laboratory for Applied Genome Science, Clinical Genome Informatics Center, Kobe University Graduate School of Medicine, Kobe, Japan. ytakaoka@med.kobe-u.ac.jp
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Takaoka
authors.forename: Mika
authors.initials: M
authors.lastname: Ohta
authors.forename: Akihiko
authors.initials: A
authors.lastname: Ito
authors.forename: Kunihiko
authors.initials: K
authors.lastname: Takamatsu
authors.forename: Aki
authors.initials: A
authors.lastname: Sugano
authors.forename: Kotaro
authors.initials: K
authors.lastname: Funakoshi
authors.forename: Nobuo
authors.initials: N
authors.lastname: Takaoka
authors.forename: Nobuko
authors.initials: N
authors.lastname: Sato
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Yokozaki
authors.forename: Naoki
authors.initials: N
authors.lastname: Arizono
authors.forename: Shuji
authors.initials: S
authors.lastname: Goto
authors.forename: Eiichi
authors.initials: E
authors.lastname: Maeda
mesh_terms: D000818:Animals; D001483:Base Sequence; D049109:Cell Proliferation; D017931:DNA Primers; D015671:Electroacupuncture; D005786:Gene Expression Regulation; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018482:Muscle, Skeletal / Q000166:cytology / Q000378:metabolism* / Q000502:physiology; D055435:Myostatin; D012333:RNA, Messenger / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014158:Transcription, Genetic; D016212:Transforming Growth Factor beta / Q000235:genetics*
chemical_list: D017931:DNA Primers; C525911:MSTN protein, human; C525912:Mstn protein, mouse; D055435:Myostatin; D012333:RNA, Messenger; D016212:Transforming Growth Factor beta