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Palmitic Acid Treatment Decreases C2C12 Myoblasts Proliferation Rates through a G2 cell cycle shift
Author(s) -
Peterson Jonathan M,
Bryner Randy W,
Alway Stephen E
Publication year - 2008
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.22.1_supplement.958.10
Subject(s) - propidium iodide , protein kinase b , palmitic acid , chemistry , cell growth , myocyte , cell cycle , apoptosis , c2c12 , endocrinology , medicine , microbiology and biotechnology , biochemistry , biology , fatty acid , programmed cell death , myogenesis
Metabolites of palmitate, i.e. ceramide, may have a number of detrimental effects. The purpose of this study was to determine if palmitic acid would have a negative effect on myoblast proliferation and Akt activation. Myoblasts were grown treated with 0.50 mM palmitate in 2% BSA for 12 hours; Laurate and BSA only were used as controls. Proliferation was determined by exposing the myoblasts to CFSE; CFSE fluorescent intensity is reduced in half each time the cell divides. Immunoblot analysis revealed that palmitate resulted in a ~50% reduction in Akt protein expression and ~65% reduction in the amount of Akt phosphorylated at ser473 compared to both BSA and laurate treated controls. In addition, FACS analysis of CSFE intensity demonstrated that palmitate treatment decreased myoblast proliferation by 33 + 6% compared to BSA only control and 24 + 2% compared to laurate treated myoblasts (p < 0.01). Furthermore, FACS analysis of propidium iodide staining demonstrated that there was greater than two‐fold increase in the percent of cells in the G2 phase of cell cycle with palmitate treatment compared to either of the control treatments. These data demonstrate that palmitate treatment reduced Akt activation, as indicated by decreased serine 473 phosphorylation, reduced myoblast proliferation, and caused a G2 shift in the cell cycle progression.