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MiR-145 reduces the activity of PI3K/Akt and MAPK signaling pathways and inhibits adipogenesis in bovine preadipocytes

机译:miR-145减少了PI3K / AKT和MAPK信号传导途径的活性,并抑制牛前脂肪细胞的脂肪组织

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Adipose tissue is the largest metabolic organ because of adipogenesis controlled by numerous miRNAs. MiR-145 is classified into the same cluster with famous miR-143. However, few studies have investigated the role of miR145 in adipogenesis. In the current study, we observed that the expression of miR-145 was downregulated during bovine adipogenesis in vivo and in vitro. The results of RNA-Seq analysis showed that miR-145 mainly disturb the PI3K/Akt and MAPK signaling pathways in bovine preadipocytes. MiR-145 inhibited bovine preadipocyte differentiation and downregulated phosphorylation level of Akt and ERK1/2 proteins. Furthermore, insulin, as a powerful inducer initiating adipogenesis and an activator of the PI3K/Akt and MAPK signaling pathways, was able to rescue the downregulation of Akt and ERK1/2 phosphorylation levels caused by miR-145. Taken together, our findings suggest that miR-145 is a potent inhibitor of adipogenesis that may function by reducing the activity of PI3K/Akt and MAPK signaling pathways.
机译:由于众多MiRNA控制,脂肪组织是最大的代谢器官。 MiR-145分为着名的MIR-143的同一群集。然而,很少有研究已经研究了miR145在脂肪发生中的作用。在目前的研究中,我们观察到MiR-145的表达在体内和体外牛脂肪发生期间下调。 RNA-SEQ分析结果表明,MIR-145主要扰乱牛前脂肪细胞中的PI3K / AKT和MAPK信号传导途径。 miR-145抑制牛普齐纤维的分化和下调Akt和Erk1 / 2蛋白的磷酸化水平。此外,作为一种强大的诱导剂引发脂肪发生和PI3K / AKT和MAPK信号传导途径的激活剂,胰岛素能够拯救由miR-145引起的AKT和ERK1 / 2磷酸化水平的下调。我们的研究结果表明MiR-145是一种有效的脂肪生成抑制剂,其可以通过减少PI3K / AKT和MAPK信号通路的活性来起作用。

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