微小RNA-378a-3p通过靶向丝裂原活化蛋白激酶1增强脂肪生成。
MiR-378a-3p enhances adipogenesis by targeting mitogen-activated protein kinase 1.
作者信息
Huang Nunu, Wang Jiu, Xie Weidong, Lyu Qing, Wu Jiangbin, He Jie, Qiu Wei, Xu Naihan, Zhang Yaou
机构信息
School of Life Sciences, Tsinghua University, Beijing 100084, PR China; Key Lab in Healthy Science and Technology, Division of Life Science, Graduate School at Shenzhen, Tsinghua University, Shenzhen 518055, PR China.
Key Lab in Healthy Science and Technology, Division of Life Science, Graduate School at Shenzhen, Tsinghua University, Shenzhen 518055, PR China.
出版信息
Biochem Biophys Res Commun. 2015 Jan 30;457(1):37-42. doi: 10.1016/j.bbrc.2014.12.055. Epub 2014 Dec 18.
Previous studies showed that miR-378a plays important roles in adipogenesis and obesity; however, the precise mechanisms of action remain unknown. Here, we found that miR-378a-3p expression is up-regulated in adipose tissues of high fat diet-induced obese mice, as well as during the differentiation of 3T3-L1 preadipocytes. Mir-378a-3p induced adipogenesis by targeting mitogen-activated protein kinase 1 (MAPK1). Overexpression of miR-378a-3p or silencing MAPK1 reduced MAPK1 expression and enhanced adipogenesis, whereas blockage of endogenous miR-378a-3p had the opposite effect, suggesting that miR-378a-3p promotes the adipogenesis of 3T3-L1 cells by targeting MAPK1.
先前的研究表明，miR-378a在脂肪生成和肥胖中发挥重要作用；然而，其确切的作用机制仍不清楚。在此，我们发现，在高脂饮食诱导的肥胖小鼠的脂肪组织中以及在3T3-L1前脂肪细胞分化过程中，miR-378a-3p的表达上调。Mir-378a-3p通过靶向丝裂原活化蛋白激酶1（MAPK1）诱导脂肪生成。miR-378a-3p的过表达或MAPK1的沉默降低了MAPK1的表达并增强了脂肪生成，而内源性miR-378a-3p的阻断则产生相反的效果，这表明miR-378a-3p通过靶向MAPK1促进3T3-L1细胞的脂肪生成。
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