PMID- 30988734
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200929
IS  - 1792-0981 (Print)
IS  - 1792-1015 (Electronic)
IS  - 1792-0981 (Linking)
VI  - 17
IP  - 5
DP  - 2019 May
TI  - miRNA-214 suppresses oxidative stress in diabetic nephropathy via the 
      ROS/Akt/mTOR signaling pathway and uncoupling protein 2.
PG  - 3530-3538
LID - 10.3892/etm.2019.7359 [doi]
AB  - 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.
FAU - Yang, Shufang
AU  - Yang S
AD  - Department of Endocrinology, Taizhou People's Hospital, Fifth People's Hospital 
      of Nantong University, Taizhou, Jiangsu 225300, P.R. China.
FAU - Fei, Xiaoqiang
AU  - Fei X
AD  - Department of Endocrinology, Taizhou People's Hospital, Fifth People's Hospital 
      of Nantong University, Taizhou, Jiangsu 225300, P.R. China.
FAU - Lu, Yu
AU  - Lu Y
AD  - Department of Endocrinology, Taizhou People's Hospital, Fifth People's Hospital 
      of Nantong University, Taizhou, Jiangsu 225300, P.R. China.
FAU - Xu, Bangkui
AU  - Xu B
AD  - Department of Endocrinology, Taizhou People's Hospital, Fifth People's Hospital 
      of Nantong University, Taizhou, Jiangsu 225300, P.R. China.
FAU - Ma, Yongmei
AU  - Ma Y
AD  - Department of Endocrinology, Taizhou People's Hospital, Fifth People's Hospital 
      of Nantong University, Taizhou, Jiangsu 225300, P.R. China.
FAU - Wan, Hui
AU  - Wan H
AD  - Department of Endocrinology, Wuxi Second People's Hospital, Wuxi, Jiangsu 214000, 
      P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20190307
PL  - Greece
TA  - Exp Ther Med
JT  - Experimental and therapeutic medicine
JID - 101531947
PMC - PMC6447795
OTO - NOTNLM
OT  - Akt
OT  - UCP2
OT  - diabetic nephropathy
OT  - mammalian target of rapamycin
OT  - microRNA-214
OT  - reactive oxygen species
EDAT- 2019/04/17 06:00
MHDA- 2019/04/17 06:01
PMCR- 2019/03/07
CRDT- 2019/04/17 06:00
PHST- 2018/03/28 00:00 [received]
PHST- 2018/09/06 00:00 [accepted]
PHST- 2019/04/17 06:00 [entrez]
PHST- 2019/04/17 06:00 [pubmed]
PHST- 2019/04/17 06:01 [medline]
PHST- 2019/03/07 00:00 [pmc-release]
AID - ETM-0-0-7359 [pii]
AID - 10.3892/etm.2019.7359 [doi]
PST - ppublish
SO  - Exp Ther Med. 2019 May;17(5):3530-3538. doi: 10.3892/etm.2019.7359. Epub 2019 Mar 
      7.