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首页> 外文期刊>Hormone and Metabolic Research >miR-381 Targets KCTD15 to Regulate Bovine Preadipocyte Differentiation In Vitro
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miR-381 Targets KCTD15 to Regulate Bovine Preadipocyte Differentiation In Vitro

机译:miR-381靶向kctd15调节牛磅上脂肪细胞分化体外分化

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MicroRNAs (miRNAs) are small, single-stranded, noncoding RNAs ~21 to ~23 nucleotides in length and have become a popular research topic in recent years due to their regulation of gene expression and many physiological processes, including fat metabolism; however, the precise functional mechanisms underlying their regulation of fat metabolism are not fully understood. Here, we identified miR-381, which specifically targets the 3′ untranslated region (3′ UTR) of potassium channel tetramerization-domain-containing 15 (KCTD15) , and verified the mechanism regulating its expression and participation in adipogenesis. We used a dual luciferase-reporter assay and transfection-mediated miR-381 overexpression and inhibition in Yanbian yellow cattle preadipocytes to investigate the role of miR-381 in adipogenesis. The results showed that miR-381 directly targets the 3′ UTR of KCTD15 and downregulates its expression. Additionally, miR-381 overexpression using an miRNA mimic promoted triglyceride accumulation and upregulated adipogenic peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT enhancer-binding protein α (C/EBPα) at both the protein and mRNA levels, whereas miR-381 inhibition produced the opposite effect. These results indicated that miR-381 regulates the differentiation of Yanbian yellow cattle preadipocytes by inhibiting KCTD15 expression, thereby highlighting the importance of miRNA-mediated regulation of adipogenesis. Furthermore, our findings suggested that miR-381 and its target gene(s) might represent new targets for investigating intramuscular fat deposits in cattle and treating human obesity.
机译:MicroRNAs(miRNAs)是长度约为21至23个核苷酸的小的单链非编码RNAs,由于其调节基因表达和包括脂肪代谢在内的许多生理过程,近年来已成为一个热门研究课题;然而,它们调节脂肪代谢的确切功能机制尚不完全清楚。在这里,我们鉴定了miR-381,其特异性靶向含有15(KCTD15)的钾通道四聚结构域的3′非翻译区(3′UTR),并验证了调节其表达和参与脂肪生成的机制。我们使用双荧光素酶报告分析和转染介导的miR-381在延边黄牛前脂肪细胞中的过度表达和抑制来研究miR-381在脂肪生成中的作用。结果表明,miR-381直接靶向KCTD15的3′UTR并下调其表达。此外,在蛋白质和mRNA水平上,使用miRNA模拟物的miR-381过表达促进甘油三酯积累,并上调脂肪生成过氧化物酶体增殖物激活受体γ(PPARγ)和CCAAT增强子结合蛋白α(C/EBPα),而miR-381抑制产生相反的效果。这些结果表明,miR-381通过抑制KCTD15的表达来调节延边黄牛前脂肪细胞的分化,从而突出了miRNA介导的脂肪生成调节的重要性。此外,我们的研究结果表明,miR-381及其靶基因可能是研究牛肌肉内脂肪沉积和治疗人类肥胖的新靶点。

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