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Identification and Characterization of Ovarian Tumor Protease Domain Containing 1 (OTUD1) in Skeletal Muscle
Author(s) -
Wortherly Keri,
Waddell David
Publication year - 2019
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.2019.33.1_supplement.700.22
Subject(s) - myogenesis , muscle atrophy , skeletal muscle , denervation , atrophy , biology , myocyte , myostatin , microarray analysis techniques , endocrinology , medicine , gene expression , gene , genetics
Skeletal muscle atrophy is a physiological condition that is caused by an array of conditions, including immobilization, denervation, spinal cord injury and corticosteroid use and results in decreased muscle size and strength. The molecular genetic events of neurogenic atrophy were analyzed in a previous study using gastrocnemius muscle isolated from mice following 3 days and 14 days of sciatic nerve denervation. The gene expression profile in the denervated muscle tissue was analyzed by microarray and compared to control muscle tissue to identify novel neurogenic atrophy‐induced genes. The microarray data revealed for the first time that Ovarian Tumor Protease Domain OTUD1 is expressed in skeletal muscle and is differentially regulated in response to denervation. OTUD1 is a deubiquitinase that has been linked to TGF‐β signaling in cancer via deubiquitination of Smad7. To confirm that OTUD1 is expressed in muscle, quantitative PCR (qPCR) was used to assess OTUD1 expression levels in both proliferating and differentiated muscle cells and the results demonstrate that expression levels appear to remain relatively constant in proliferating myoblasts and differentiated myotubes. Furthermore, Western blot analysis supported the qPCR data and showed that OTUD1 protein levels remain relatively constant as cultured myoblasts differentiate to myotubes. The discovery that OTUD1 is differentially regulated in response to neurogenic atrophy helps further our understanding of the molecular genetic events of muscle wasting and may eventually lead to the identification of new therapeutic targets for the treatment and prevention of atrophy. Support or Funding Information The work was support by University of North Florida Transformational Learning Opportunity grants and a University of North Florida Foundation Board Grant to D.W. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .