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Growth Arrest Specific 6 Activates Akt and ERK in Cultured Skeletal Muscle
Author(s) -
Olsen Esther K.,
Doxey Stephen A.,
Chow Joshua L.Y.,
Duplisea Michael,
Thomson David M.
Publication year - 2017
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.31.1_supplement.1022.10
Subject(s) - myogenesis , protein kinase b , skeletal muscle , mapk/erk pathway , pi3k/akt/mtor pathway , myocyte , phosphorylation , microbiology and biotechnology , c2c12 , cell growth , endocrinology , biology , medicine , chemistry , signal transduction , biochemistry
Growth arrest specific 6 (Gas6) is a signaling factor that is found in a variety of tissues and is thought to be involved in the regulation of cell proliferation through activation of AKT and/or ERK signaling pathways. Its effect on skeletal muscle cells is unknown. Therefore, to test if Gas6 activates AKT and ERK in skeletal muscle, we incubated C2C12 myoblasts and myotubes with 0 to 800 ng/ml of Gas6 for 15 minutes. The cells were lysed and AKT and ERK content and phosphorylation were measured by western blotting. We found that in myoblasts Gas6 significantly increased ERK, but not AKT phosphorylation at an optimal concentration of 100 ng/ml. In myotubes, Gas6 significantly increased AKT but not ERK phosphorylation, also at an optimal concentration of 100 ng/ml. Our findings indicate that Gas6 is able to regulate these pathways in skeletal muscle and/or skeletal muscle progenitor cells. This suggests that Gas6 may be useful in conditions where muscle growth and/or satellite cell proliferation are impaired such as diabetes and old age. Support or Funding Information This work was supported by a Brigham Young University Gerontology Program Grant.