1. Academic Validation
  2. miRNA-214 suppresses oxidative stress in diabetic nephropathy via the ROS/Akt/mTOR signaling pathway and uncoupling protein 2

miRNA-214 suppresses oxidative stress in diabetic nephropathy via the ROS/Akt/mTOR signaling pathway and uncoupling protein 2

  • Exp Ther Med. 2019 May;17(5):3530-3538. doi: 10.3892/etm.2019.7359.
Shufang Yang 1 Xiaoqiang Fei 1 Yu Lu 1 Bangkui Xu 1 Yongmei Ma 1 Hui Wan 2
Affiliations

Affiliations

  • 1 Department of Endocrinology, Taizhou People's Hospital, Fifth People's Hospital of Nantong University, Taizhou, Jiangsu 225300, P.R. China.
  • 2 Department of Endocrinology, Wuxi Second People's Hospital, Wuxi, Jiangsu 214000, P.R. China.
Abstract

In the present study, the function of MicroRNA (miR)-214 on diabetic nephropathy (DN) and diabetes of proximal tubular cells was investigated. Reverse transcription-quantitative polymerase chain reaction was used measure the expression of miR-214 in rats with DN and ELISA was performed to measure oxidative stress and ROS levels. Results indicated that miR-214 expression in the peripheral blood was significantly decreased in rats with DN. The in vitro model of DN indicated that miR-214 upregulation significantly decreased oxidative stress and Reactive Oxygen Species (ROS) levels, but significantly increased uncoupling protein 2 (UCP2), phosphorylated (p)-Akt and p-mammalian target of rapamycin (mTOR) protein expression levels. The administration of genipin, a UCP2 inhibitor, significantly attenuated the effects of miR-214 upregulation on oxidative stress in the in vitro DN model by regulating ROS, Akt and mTOR protein expression levels. Notably, Akt Inhibitor suppressed p-Akt protein expression and attenuated the effects of miR-214 upregulation on oxidative stress in the in vitro DN model. Collectively, these data suggest that miR-214 regulates diabetes through a ROS/Akt/mTOR signaling pathway by UCP2 in proximal tubular cells.

Keywords

Akt; UCP2; diabetic nephropathy; mammalian target of rapamycin; microRNA-214; reactive oxygen species.

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