The mERG1a channel modulates skeletal muscle MuRF1, but not MAFbx, expression

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Abstract
Introduction: We investigated the mechanism by which the MERG1a K+ channel increases ubiquitin proteasome proteolysis (UPP). Methods: Hindlimb suspension and electro‐transfer of Merg1a cDNA into mouse gastrocnemius muscles induced atrophy. Results: Atrophic gastrocnemius muscles of hindlimb‐suspended mice express Merg1a, Murf1, and Mafbx genes. Electrotransfer of Merg1a significantly decreases muscle fiber size (12.6%) and increases UPP E3 ligase Murf1 mRNA (2.1‐fold) and protein (23.7%), but does not affect Mafbx E3 ligase expression. Neither Merg1a‐induced decreased fiber size nor Merg1a‐induced increased Murf1 expression is curtailed significantly by coexpression of inactive HR‐Foxo3a, a gene encoding a transcription factor known to induce Mafbx expression. Conclusions: The MERG1a K+ channel significantly increases expression of Murf1, but not Mafbx. We explored this expression pattern by expressing inactive Foxo3a and showing that it is not involved in MERG1a‐mediated expression of Murf1. These findings suggest that MERG1a may not modulate Murf1 expression through the AKT/FOXO pathway. Muscle Nerve 49:378–388, 2014
Funding Information
  • National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health, (1R03AR053706-01A2)

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