Du Hechun, Fu Zimu, He Guohua, Wang Yuejuan, Xia Guiyu, Fang Min, Zhang Tao
Shaoxing Women and Children's Hospital, Shaoxing, Zhejiang 312000, P.R. China.
Women's Hospital, School of Medicine, Zhejiang University, Hangzhou 310058, P.R. China.
Mol Med Rep. 2015 Jun;11(6):4701-5. doi: 10.3892/mmr.2015.3282. Epub 2015 Jan 30.
Adiponectin exerts an antidiabetic function through the adiponectin receptors 1 and 2 (AdipoR1 and AdipoR2). The mechanism regulating the expression of adiponectin receptors remains to be elucidated. Bioinformatics analysis demonstrated that microRNA (miR)‑218 targets the 3' untranslated region (3'UTR) of the AdipoR2 mRNA. The present study aimed to investigate whether miR-218 regulated the expression of AdipoR2 using immunoblotting, reverse transcription quantitative polymerase chain reaction and luciferase assays. The protein level and the mRNA level of AdipoR2 were reduced when miR‑218 was expressed in HepG2 cells. Additionally, overexpression of miR‑218 repressed the activity of a luciferase reporter containing the 3'UTR of AdipoR2. Furthermore, the present study aimed to determine whether miR-218 regulated glucose metabolism through detecting signaling pathways and glucose uptake. The phosphorylation of AMP‑activated protein kinase and p38 mitogen‑activated protein kinase was reduced in miR‑218‑expressing cells. In addition, miR‑218 inhibited adiponectin‑induced glucose uptake. The present results suggested that miR‑218 targets AdipoR2 to inhibit adiponectin signaling.
脂联素通过脂联素受体1和2（AdipoR1和AdipoR2）发挥抗糖尿病功能。调节脂联素受体表达的机制仍有待阐明。生物信息学分析表明，微小RNA（miR）-218靶向AdipoR2 mRNA的3'非翻译区（3'UTR）。本研究旨在通过免疫印迹、逆转录定量聚合酶链反应和荧光素酶测定法研究miR-218是否调节AdipoR2的表达。当miR-218在HepG2细胞中表达时，AdipoR2的蛋白水平和mRNA水平降低。此外，miR-218的过表达抑制了含有AdipoR2 3'UTR的荧光素酶报告基因的活性。此外，本研究旨在通过检测信号通路和葡萄糖摄取来确定miR-218是否调节葡萄糖代谢。在表达miR-218的细胞中，AMP活化蛋白激酶和p38丝裂原活化蛋白激酶的磷酸化水平降低。此外，miR-218抑制脂联素诱导的葡萄糖摄取。本研究结果表明，miR-218靶向AdipoR2以抑制脂联素信号传导。
