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

  • Authors:
    • Shufang Yang
    • Xiaoqiang Fei
    • Yu Lu
    • Bangkui Xu
    • Yongmei Ma
    • Hui Wan
  • View Affiliations / Copyright

    Affiliations: Department of Endocrinology, Taizhou People's Hospital, Fifth People's Hospital of Nantong University, Taizhou, Jiangsu 225300, P.R. China, Department of Endocrinology, Wuxi Second People's Hospital, Wuxi, Jiangsu 214000, P.R. China
    Copyright: © Yang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 3530-3538
    |
    Published online on: March 7, 2019
       https://doi.org/10.3892/etm.2019.7359
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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.
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Copy and paste a formatted citation
Spandidos Publications style
Yang S, Fei X, Lu Y, Xu B, Ma Y and Wan H: miRNA‑214 suppresses oxidative stress in diabetic nephropathy via the ROS/Akt/mTOR signaling pathway and uncoupling protein 2. Exp Ther Med 17: 3530-3538, 2019.
APA
Yang, S., Fei, X., Lu, Y., Xu, B., Ma, Y., & Wan, H. (2019). miRNA‑214 suppresses oxidative stress in diabetic nephropathy via the ROS/Akt/mTOR signaling pathway and uncoupling protein 2. Experimental and Therapeutic Medicine, 17, 3530-3538. https://doi.org/10.3892/etm.2019.7359
MLA
Yang, S., Fei, X., Lu, Y., Xu, B., Ma, Y., Wan, H."miRNA‑214 suppresses oxidative stress in diabetic nephropathy via the ROS/Akt/mTOR signaling pathway and uncoupling protein 2". Experimental and Therapeutic Medicine 17.5 (2019): 3530-3538.
Chicago
Yang, S., Fei, X., Lu, Y., Xu, B., Ma, Y., Wan, H."miRNA‑214 suppresses oxidative stress in diabetic nephropathy via the ROS/Akt/mTOR signaling pathway and uncoupling protein 2". Experimental and Therapeutic Medicine 17, no. 5 (2019): 3530-3538. https://doi.org/10.3892/etm.2019.7359
Copy and paste a formatted citation
x
Spandidos Publications style
Yang S, Fei X, Lu Y, Xu B, Ma Y and Wan H: miRNA‑214 suppresses oxidative stress in diabetic nephropathy via the ROS/Akt/mTOR signaling pathway and uncoupling protein 2. Exp Ther Med 17: 3530-3538, 2019.
APA
Yang, S., Fei, X., Lu, Y., Xu, B., Ma, Y., & Wan, H. (2019). miRNA‑214 suppresses oxidative stress in diabetic nephropathy via the ROS/Akt/mTOR signaling pathway and uncoupling protein 2. Experimental and Therapeutic Medicine, 17, 3530-3538. https://doi.org/10.3892/etm.2019.7359
MLA
Yang, S., Fei, X., Lu, Y., Xu, B., Ma, Y., Wan, H."miRNA‑214 suppresses oxidative stress in diabetic nephropathy via the ROS/Akt/mTOR signaling pathway and uncoupling protein 2". Experimental and Therapeutic Medicine 17.5 (2019): 3530-3538.
Chicago
Yang, S., Fei, X., Lu, Y., Xu, B., Ma, Y., Wan, H."miRNA‑214 suppresses oxidative stress in diabetic nephropathy via the ROS/Akt/mTOR signaling pathway and uncoupling protein 2". Experimental and Therapeutic Medicine 17, no. 5 (2019): 3530-3538. https://doi.org/10.3892/etm.2019.7359
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