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微小RNA-185通过靶向固醇调节元件结合蛋白-1抑制3T3-L1细胞分化。

MiR-185 inhibits 3T3-L1 cell differentiation by targeting SREBP-1.

作者信息

Ning Chunyou, Li Guilin, You Lu, Ma Yao, Jin Long, Ma Jideng, Li Xuewei, Li Mingzhou, Liu Haifeng

机构信息

a Farm Animal Genetic Resources Exploration and Innovation Key Laboratory of Sichuan Province , Sichuan Agricultural University , Chengdu , China.

出版信息

Biosci Biotechnol Biochem. 2017 Sep;81(9):1747-1754. doi: 10.1080/09168451.2017.1347485. Epub 2017 Jul 13.

Abstract

Adipogenesis involves a highly orchestrated series of complex events in which microRNAs (miRNAs) may play an essential role. In this study, we found that the miR-185 expression increased gradually during 3T3-L1 cells differentiation. To explore the role of miR-185 in adipogenesis, miRNA agomirs and antagomirs were used to perform miR-185 overexpression and knockdown, respectively. Overexpression of miR-185 dramatically reduced the mRNA expression of the adipogenic markers, PPARγ, FABP4, FAS, and LPL, and the protein level of PPARγ and FAS. MiR-185 overexpression also led to a notable reduction in lipid accumulation. In contrast, miR-185 inhibition promoted differentiation of 3T3-L1 cells. By target gene prediction and luciferase reporter assay, we demonstrated that sterol regulatory element binding protein 1 (SREBP-1) may be the target of miR-185. These results indicate that miR-185 negatively regulates the differentiation of 3T3-L1 cells by targeting SREBP-1, further highlighting the importance of miRNAs in adipogenesis.

摘要

脂肪生成涉及一系列高度协调的复杂事件,其中微小RNA(miRNA)可能发挥重要作用。在本研究中,我们发现miR-185在3T3-L1细胞分化过程中表达逐渐增加。为了探究miR-185在脂肪生成中的作用,分别使用miRNA激动剂和拮抗剂进行miR-185的过表达和敲低。miR-185的过表达显著降低了脂肪生成标志物PPARγ、FABP4、FAS和LPL的mRNA表达,以及PPARγ和FAS的蛋白水平。miR-185的过表达还导致脂质积累显著减少。相反,miR-185抑制促进了3T3-L1细胞的分化。通过靶基因预测和荧光素酶报告基因检测,我们证明固醇调节元件结合蛋白1(SREBP-1)可能是miR-185的靶标。这些结果表明,miR-185通过靶向SREBP-1负向调节3T3-L1细胞的分化,进一步凸显了miRNA在脂肪生成中的重要性。

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