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TRAF6 is critical for Satellite cell function and skeletal muscle regeneration upon injury (LB815)
Author(s) -
Hindi Sajedah,
Kumar Ashok
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.lb815
Subject(s) - myf5 , myod , myogenin , skeletal muscle , regeneration (biology) , microbiology and biotechnology , progenitor cell , myod protein , myocyte , biology , stem cell , medicine , endocrinology , myogenesis
Skeletal muscle satellite cells are a subpopulation of muscle‐stem cells responsible for carrying out muscle regenerative events. Paired box‐protein Pax7 has been shown to be indispensable for driving proper regeneration as well as supplementing the reservoir of satellite‐cell pool. However, signaling mechanisms that regulate the expression of Pax7 remain less understood. In the present study, we demonstrate that TNF receptor‐associated factor 6 (TRAF6) positively regulates the expression of Pax7 in vivo and in vitro. Deletion of TRAF6 under a tamoxifen‐induced Pax7 promoter led to profound muscle regeneration defects following BaCl2‐mediated injury. Regenerating muscle of tamoxifen‐administered mice failed to up‐regulate Pax7 and displayed a significant reduction in Myf5 transcript levels with no effect on MyoD, myogenin, Mhc3 and Mhc4 compared with vehicle‐administered mice. Similarly, cultured muscle progenitors lacking TRAF6 also displayed a significant reduction in Pax7 expression limiting their proliferative capacity. Deletion of TRAF6 had no effect on myotube formation when cells where plated at high density. Collectively, our study reveals an unprecedented requirement of TRAF6 in regulating Pax7 function in adult skeletal muscle. Grant Funding Source : Supported by NIH R01AR059810