Competing interestsNo potential conflict of interest relevant to this article was reported. Funding sourcesState funding sources (grants, funding sources, equipment, and supplies). Include name and number of grant if available.
Background: Ciglitazone is a member of the thiazolidinedione (TZD) family, and specifically binds to peroxisome proliferator-activated receptor-γ (PPARγ) , thereby promoting adipocyte differentiation. We hypothesized that ciglitazone as a PPARγ ligand in the absence of an adipocyte differentiation cocktail would increase adiponectin and adipogenic gene expression in bovine satellite cells (BSC).Methods: Muscle-derived bovine satellite cells were isolated from six, 18-month-old Yanbian Yellow Cattle. The BSC were cultured for 96 h in differentiation medium containing 5 µM ciglitazone (CL), 10 µM ciglitazone (CM), or 20 µM ciglitazone (CH). Control (CON) BSC were cultured only in differentiation medium (containing 2% horse serum).Results: The presence of myogenin, desmin, and paired box 7 (Pax7) proteins were confirmed in the BSC by immunofluorescence staining. The CL, CM, and CH treatments produced higher concentrations of triacylglycerol and lipid droplet accumulation in myotubes than those of the CON treatment. Ciglitazone treatments significantly increased the relative expression of PPARγ , CCAAT/enhancer-binding protein alpha (C/EBPα), C/EBPβ, fatty acid synthase stearoyl-CoA desaturase (SCD) and perilipin 2. Ciglitazone treatments increased gene expression of paired box 3 (Pax3) and Pax7 and decreased expression of myogenic differentiation-1, myogenin, myogenic regulatory factor-5 (MRF5), and MYF4 (P < 0.01). Adiponectin concentration caused by ciglitazone treatments was significantly greater than CON (P < 0.01). RNA sequencing showed that 281 differentially expressed genes (DEGs) were found in the treatments of ciglitazone. DEGs gene ontology (GO) analysis showed that the top 10 GO enrichment significantly changed the biological processes such as protein trimerization, negative regulation of cell proliferation, adipocytes differentiation, and cellular response to external stimulus. KEGG pathway analysis showed that DEGs were involved into p53 signaling pathway, PPAR signaling pathway, biosynthesis of amino acids, TNF signaling pathway, non-alcoholic fatty liver disease (NAFLD), PI3K-Akt signaling pathway, and Wnt signaling pathway.Conclusion: These results indicate that ciglitazone acts as PPARγ agonist, effectively increasing the adiponectin concentration and adipogenic gene expression, and stimulating the conversion of BSC to adipocyte-like cells in the absence of adipocyte differentiation cocktail.
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