Premium
The regulation of muscle growth by miR‐23a
Author(s) -
Beach Cassandra Lynn,
Petrocelli Jonathan,
Stott Nicole,
Marino Joseph
Publication year - 2018
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.2018.32.1_supplement.752.1
Subject(s) - myogenesis , c2c12 , skeletal muscle , microrna , myosin , myocyte , microbiology and biotechnology , transfection , palmitic acid , biology , messenger rna , gene expression , chemistry , fatty acid , gene , biochemistry , endocrinology
Background Micro‐RNAs (miRNAs) are a class of small, non‐protein coding RNAs that posttranscriptionally regulate gene expression through the degradation or translational inhibition of their target complimentary messenger RNAs (mRNAs). Developing evidence indicates the importance of miRNAs in the myogenic program and their influence on disorders affecting muscle growth and metabolism. Purpose The purpose of this study was to determine whether miR23a regulates myotube formation in skeletal muscle under lipid‐induced atrophic conditions. Methods C2C12 myoblasts were transfected with a mimic complex to increase levels of miR23a or vehicle at seeding, then induced to differentiate into myotubes. Cells were treated with palmitic acid (0.1mM) at day 0 and day 2 of differentiation. Cells were collected at day 4 of differentiation. Real‐time PCR was used to investigate changes in miRNA expression and myosin heavy chain staining was performed to determine differences in myotube formation. Results Cells that received mimic had increases in miR‐23a levels. Palmitic acid‐induced reductions in myotube formation were abrogated with overexpression of miR‐23a. Conclusions These data suggest that miR23a may exist in a regulatory pathway that alters muscle growth in the presences of saturated fatty acid. Future work is ongoing to understand the mechanisms by which miR23a may regulate skeletal muscle growth under lipid‐induced atrophic conditions. Support or Funding Information Faculty Research Grant This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .