Abstract：
Preadipocytes become mature adipocytes after proliferation and differentiation, and although many genes and microRNAs have been identified in intramuscular fat, their physiological function and regulatory mechanisms remain largely unexplored. miR-26a-5p has been reported to be related to fat deposition, but its effect on porcine preadipocyte differentiation has not been explored. In this study, bioinformatics analysis and luciferase reporter assay identified that miR-26a-5p binds to the 3\'UTR of Acyl-CoA synthetase long-chain family member 3 (ACSL3) mRNA. The model for porcine intramuscular preadipocyte differentiation was established to explore the function of miR-6a-5p-ACSL3 on adipocyte differentiation. ACSL3 knockdown markedly reduced the triglycerides (TG) content of cells, as well as the mRNA levels of adipogenic marker genes (PPAR-γ and SREBP-1c). The number of lipid droplets in cells transfected with a miR-26a-5p mimic is significantly reduced, consistent with ACSL3 knockdown results, while the miR-26a-5p inhibitor resulted in opposite results. Taken together, miR-26a-5p is a repressor of porcine preadipocyte differentiation and plays a vital role in ACSL3-mediated adipogenesis.
摘要：
前脂肪细胞在增殖和分化后成为成熟的脂肪细胞，尽管已经在肌内脂肪中鉴定出许多基因和microRNA，它们的生理功能和调节机制在很大程度上仍未被探索。据报道，miR-26a-5p与脂肪沉积有关，但其对猪前脂肪细胞分化的影响尚未被研究。在这项研究中,生物信息学分析和荧光素酶报告基因分析确定miR-26a-5p与酰基辅酶A合成酶长链家族成员3(ACSL3)mRNA的3UTR结合。建立猪肌内前脂肪细胞分化模型,探讨miR-6a-5p-ACSL3在脂肪细胞分化中的作用。ACSL3敲低显著降低了细胞的甘油三酯（TG）含量，以及成脂标记基因（PPAR-γ和SREBP-1c）的mRNA水平。转染miR-26a-5p模拟物的细胞中的脂滴数量显著减少，与ACSL3敲低结果一致，而miR-26a-5p抑制剂导致相反的结果。一起来看,miR-26a-5p是猪前脂肪细胞分化的阻遏物，在ACSL3介导的脂肪生成中起重要作用。
