MicroRNA-492 reverses high glucose-induced insulin resistance in HUVEC cells through targeting resistin
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- 作者：Cai Ying (1)
Liu Sui-xin (1)
Xie Kang-ling (1)
Zhang Wen-liang (1)
Dong Lei (1)
Liu Yuan (1)
Zheng Fan (1)
Zhuo Chen (1) - 关键词：miR ; 492 ; Insulin resistance ; Resistin ; Atherosclerosis
- 刊名：Molecular and Cellular Biochemistry
- 出版年：2014
- 出版时间：June 2014
- 年：2014
- 卷：391
- 期：1-2
- 页码：117-125
- 全文大小：
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Liu Sui-xin (1)
Xie Kang-ling (1)
Zhang Wen-liang (1)
Dong Lei (1)
Liu Yuan (1)
Zheng Fan (1)
Zhuo Chen (1)
1. Cardiac Rehabilitation Center, Department of Rehabilitation, Xiangya Hospital, Central South University, Xiang-Ya Road 87, Changsha, 41008, Hunan, People’s Republic of China - ISSN：1573-4919
文摘
The development of atherosclerosis (AS) is a multifactorial process, in which elevated plasma resistin (a key factor leading to insulin resistance) levels play an important role. Emerging evidence indicate that microRNAs (miRNAs) are involved in AS; However, the regulation and function of miRNAs in response to AS remain poorly understood. Our study analyzed the effects of miR-492 on insulin resistance, endothelial activation, and resistin expression in apoE knock-out mice and human umbilical vein endothelial cells after high-glucose treatment and miR-492 mimics transfection. We also investigated the underlying molecular mechanisms. Our results showed that high glucose stress induced a significant decrease in miR-492 expression, with a remarkable upregulation of resistin expression. We then identified resistin as a novel direct target of miR-492 using 3-UTR luciferase reporter assay. Histopathologic examination demonstrated that upregulation of miR-492 attenuated endothelial cells migration and lipid accumulation induced by high glucose stress. Further investigation demonstrated that the upregulation of p-STAT3, SOCS, and P-selectin activation induced by high glucose stress was attenuated by upregulation of miR-492. Together, our findings indicate that miR-492 contributes to insulin resistance and endothelial dysfunction induced by high glucose, via directly downregulating resistin expression, and involving STAT3 phosphorylation, SOCS, and P-selectin activation.