Bach1 promotes muscle regeneration through repressing Smad-mediated inhibition of myoblast differentiation.

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  • Additional Information
    • Source:
      Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
    • Publication Information:
      Original Publication: San Francisco, CA : Public Library of Science
    • Subject Terms:
    • Abstract:
      It has been reported that Bach1-deficient mice show reduced tissue injuries in diverse disease models due to increased expression of heme oxygenase-1 (HO-1)that possesses an antioxidant function. In contrast, we found that Bach1 deficiency in mice exacerbated skeletal muscle injury induced by cardiotoxin. Inhibition of Bach1 expression in C2C12 myoblast cells using RNA interference resulted in reduced proliferation, myotube formation, and myogenin expression compared with control cells. While the expression of HO-1 was increased by Bach1 silencing in C2C12 cells, the reduced myotube formation was not rescued by HO-1 inhibition. Up-regulations of Smad2, Smad3 and FoxO1, known inhibitors of muscle cell differentiation, were observed in Bach1-deficient mice and Bach1-silenced C2C12 cells. Therefore, Bach1 may promote regeneration of muscle by increasing proliferation and differentiation of myoblasts.
      Competing Interests: The authors have declared that no competing interests exist.
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    • Accession Number:
      0 (Bach1 protein, mouse)
      0 (Basic-Leucine Zipper Transcription Factors)
      0 (Smad Proteins)
    • Publication Date:
      Date Created: 20200811 Date Completed: 20201006 Latest Revision: 20201006
    • Publication Date:
      20240105
    • Accession Number:
      PMC7416950
    • Accession Number:
      10.1371/journal.pone.0236781
    • Accession Number:
      32776961