Animal Cells and Systems (Sep 2018)

Modulatory effect of linoleic and oleic acid on cell proliferation and lipid metabolism gene expressions in primary bovine satellite cells

  • Shah Ahmed Belal,
  • Allur Subramaniyan Sivakumar,
  • Da Rae Kang,
  • Sangbuem Cho,
  • Ho Sung Choe,
  • Kwan Seob Shim

DOI
https://doi.org/10.1080/19768354.2018.1517824
Journal volume & issue
Vol. 22, no. 5
pp. 324 – 333

Abstract

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This study was performed to elucidate the effects of linoleic acid (LA), oleic acid (OA) and their combination (LA + OA) on cell proliferation, apoptosis, necrosis, and the lipid metabolism related gene expression in bovine satellite cells (BSCs), isolated from bovine muscles. Cell viability was significantly increased with the OA and LA treatment. Furthermore, LA + OA enhanced cell proliferation in a dose-dependent manner (10 to 100 µM), whereas it lowered at 250 µM. In addition, a cell-cycle analysis showed that 100 µM of LA and OA markedly decreased the G0/G1 phase proportion (62.58% and 61.33%, respectively), compared to controls (68.02%), whereas the S-phase cells’ proportion was increased. The ratio of G2/M phase cells was not significantly different among the groups. Moreover, analyses with AO/EtBr staining showed that no apoptosis occurred. Necrosis were determined by flow cytometry using Annexin V-FITC/PI staining which revealed no early apoptosis in the cells pretreated with LA or OA, but occurred in the LA + OA group. We also analyzed the mRNA expression of lipid metabolizing genes such as peroxisome proliferator receptor alfa (PPARα), peroxisome proliferator receptor gamma (PPARγ), acyl-CoA oxidase (ACOX), lipoprotein lipase (LPL), carnitine palmitoyl transferase (CPT-1), and fatty-acid binding protein4 (FABP4), which were upregulated in LA or OA treated cells compared to the control group. In essence, LA and OA alone promote the cell proliferation without any apoptosis and necrosis, which might upregulate the lipid metabolism related gene expressions, and increase fatty-acid oxidation in the BSCs’ lipid metabolism.

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