PMID- 29285014
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 1611-2156 (Print)
IS  - 1611-2156 (Electronic)
IS  - 1611-2156 (Linking)
VI  - 16
DP  - 2017
TI  - microRNA-503 contribute to pancreatic beta cell dysfunction by targeting the mTOR 
      pathway in gestational diabetes mellitus.
PG  - 1177-1187
LID - 10.17179/excli2017-738 [doi]
AB  - Loss of pancreatic beta cells is involved in pathogenesis of gestational diabetes 
      mellitus (GDM). Recently, several studies have elucidated the connection between 
      microRNAs (miRNAs) and diabetes mellitus (DM), but the role of miRNAs in GDM 
      remains unclear. The aim of this study was to evaluate the potential functions of 
      miRNAs in GDM and to investigate the underlying mechanisms of action. First, we 
      explored the expression profile of miRNAs in placenta tissue from GDM patients 
      using microarray. Validation analysis was performed in peripheral blood specimens 
      using quantitative reverse transcription PCR (qRT-PCR). Then the role and 
      regulating mechanism of miR-503 in weaken the function of pancreatic beta cell was 
      investigated. We found that miR-503 was markedly upregulated in placenta tissue 
      from GDM patients, as elevated in peripheral blood specimens, and the high level 
      was positively correlated to blood glucose concentration. Knockdown of miR-503 
      enhanced insulin secretion of pancreatic beta-cells, promoted cell proliferation and 
      protected cells from apoptosis, whereas overexpression of miR-503 showed the 
      opposite effects. Furthermore, mammalian target of rapamycin (mTOR) was 
      identified as a direct target of miR-503 and mTOR silencing could reverse the 
      improving effects of miR-503 knockdown on insulin secretion and pancreatic 
      beta-cells proliferation. High expression of miR-503 in peripheral blood may be 
      acted as a diagnosis biomarker of GDM. MiR-503 regulated functions of pancreatic 
      beta-cells by targeting the mTOR pathway, suggesting that targeting miR-503/mTOR 
      axis could serve as a novel therapeutic target for GDM.
FAU - Xu, Ke
AU  - Xu K
AD  - Department of Endocrinology, Yancheng First City Hospital of Jiangsu Province, 
      Yancheng, China.
FAU - Bian, Dezhi
AU  - Bian D
AD  - Department of Endocrinology, Yancheng First City Hospital of Jiangsu Province, 
      Yancheng, China.
FAU - Hao, Lanxiang
AU  - Hao L
AD  - Department of Endocrinology, Yancheng First City Hospital of Jiangsu Province, 
      Yancheng, China.
FAU - Huang, Fei
AU  - Huang F
AD  - Department of Endocrinology, Yancheng First City Hospital of Jiangsu Province, 
      Yancheng, China.
FAU - Xu, Min
AU  - Xu M
AD  - Department of Obstetrics and Gynecology, Yancheng First City Hospital of Jiangsu 
      Province, Yancheng, China.
FAU - Qin, Jie
AU  - Qin J
AD  - Department of Pediatrics, Yancheng First City Hospital of Jiangsu Province, 
      Yancheng, China.
FAU - Liu, Yanmei
AU  - Liu Y
AD  - Department of Endocrinology, Yancheng First City Hospital of Jiangsu Province, 
      Yancheng, China.
LA  - eng
PT  - Journal Article
DEP - 20171027
PL  - Germany
TA  - EXCLI J
JT  - EXCLI journal
JID - 101299402
PMC - PMC5735340
OTO - NOTNLM
OT  - gestational diabetes mellitus
OT  - mTOR
OT  - microRNA-503
OT  - pancreatic beta-cells
EDAT- 2017/12/30 06:00
MHDA- 2017/12/30 06:01
PMCR- 2017/10/27
CRDT- 2017/12/30 06:00
PHST- 2017/08/20 00:00 [received]
PHST- 2017/10/10 00:00 [accepted]
PHST- 2017/12/30 06:00 [entrez]
PHST- 2017/12/30 06:00 [pubmed]
PHST- 2017/12/30 06:01 [medline]
PHST- 2017/10/27 00:00 [pmc-release]
AID - 2017-738 [pii]
AID - Doc1177 [pii]
AID - 10.17179/excli2017-738 [doi]
PST - epublish
SO  - EXCLI J. 2017 Oct 27;16:1177-1187. doi: 10.17179/excli2017-738. eCollection 2017.