PMID- 31695460
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20231013
IS  - 1178-7007 (Print)
IS  - 1178-7007 (Electronic)
IS  - 1178-7007 (Linking)
VI  - 12
DP  - 2019
TI  - IL6R inhibits viability and apoptosis of pancreatic beta-cells in type 2 diabetes 
      mellitus via regulation by miR-22 of the JAK/STAT signaling pathway.
PG  - 1645-1657
LID - 10.2147/DMSO.S211700 [doi]
AB  - BACKGROUND AND AIM: Type 2 diabetes mellitus (T2DM) is a common disease of 
      harming to people's health. MicroRNAs have recently been considered as key 
      regulators of many biological processes, such as cell proliferation, migration 
      and apoptosis. However, the effect of miR-22 expression by targeting IL6 receptor 
      (IL6R) in T2DM and potential molecular mechanism involved remains to be 
      elucidated. The present study aimed to explore the regulatory mechanism of miR-22 
      by targeting IL6R in pancreatic beta-cells viability and apoptosis of T2DM. 
      METHODS: The expressions of miR-22, IL6R and apolipoprotein (apoA1, apoB and 
      apoE) were examined by reverse transcription-quantitative PCR (qRT-PCR). 
      Pancreatic beta-cells were transiently transfected with a miR-22 mimic or si-IL6R 
      plasmid which validated with qRT-PCR to analyze the expression of miR-22 or IL6R. 
      Cell viability, apoptosis and protein expression levels were determined by CCK-8, 
      flow cytometry and Western blotting, respectively. RESULTS: The proportion of 
      INS-1E cell apoptosis was increased in islets of diabetic rats. Furthermore, 
      miR-22 was downregulated and IL6R was upregulated in both diabetic serum and 
      glucose-induced INS-1E cells. miR-22 overexpression or IL6R inhibition 
      significantly strengthened cell viability and reduced the expression of 
      apoptosis-related proteins to suppress cell apoptosis. IL6R was demonstrated as a 
      target gene of miR-22 which could negatively regulate IL6R expression. Moreover, 
      phosphorylation of JAK/STAT signaling pathway was activated by miR-22 
      overexpression or IL6R inhibition to strengthen the viability and suppress 
      apoptosis of INS-1E cells. CONCLUSION: This study indicated that miR-22 
      strengthened the viability and suppressed apoptosis of INS-1E cells, partly by 
      down-regulation of IL6R through the activation of JAK/STAT signaling pathway.
CI  - (c) 2019 Wu et al.
FAU - Wu, Xinhua
AU  - Wu X
AD  - Department of Endocrinology, Huaian Hospital of Huaian District, Huaian, Jiangsu 
      223200, People's Republic of China.
FAU - Yu, Tao
AU  - Yu T
AD  - Department of Endocrinology, Huaian Hospital of Huaian District, Huaian, Jiangsu 
      223200, People's Republic of China.
FAU - Ji, Ning
AU  - Ji N
AD  - Department of Endocrinology, Huaian Hospital of Huaian District, Huaian, Jiangsu 
      223200, People's Republic of China.
FAU - Huang, Yujie
AU  - Huang Y
AD  - Department of Endocrinology, Huaian Hospital of Huaian District, Huaian, Jiangsu 
      223200, People's Republic of China.
FAU - Gao, Lingcheng
AU  - Gao L
AD  - Department of Endocrinology, Huaian Hospital of Huaian District, Huaian, Jiangsu 
      223200, People's Republic of China.
FAU - Shi, Wen
AU  - Shi W
AD  - Department of Endocrinology, Huaian Hospital of Huaian District, Huaian, Jiangsu 
      223200, People's Republic of China.
FAU - Yan, Yan
AU  - Yan Y
AD  - Department of Endocrinology, Huaian Hospital of Huaian District, Huaian, Jiangsu 
      223200, People's Republic of China.
FAU - Li, Hang
AU  - Li H
AD  - Department of Endocrinology, Huaian Hospital of Huaian District, Huaian, Jiangsu 
      223200, People's Republic of China.
FAU - Ma, Liming
AU  - Ma L
AD  - Department of Endocrinology, Huaian Hospital of Huaian District, Huaian, Jiangsu 
      223200, People's Republic of China.
FAU - Wu, Kede
AU  - Wu K
AD  - Clinical Medicine, Medical College of Yangzhou University, Yangzhou, Jiangsu 
      225009, People's Republic of China.
FAU - Wu, Zhen
AU  - Wu Z
AD  - Electric Engineering, China University of Mining and Technology, Xuzhou, Jiangsu 
      221116, People's Republic of China.
LA  - eng
PT  - Journal Article
DEP - 20190829
PL  - New Zealand
TA  - Diabetes Metab Syndr Obes
JT  - Diabetes, metabolic syndrome and obesity : targets and therapy
JID - 101515585
PMC - PMC6718245
OTO - NOTNLM
OT  - IL6R
OT  - JAK/STAT signaling pathway
OT  - miR-22
OT  - pancreatic beta-cells
OT  - type 2 diabetes mellitus
COIS- The authors report no conflicts of interest in this work.
EDAT- 2019/11/07 06:00
MHDA- 2019/11/07 06:01
PMCR- 2019/08/29
CRDT- 2019/11/08 06:00
PHST- 2019/04/09 00:00 [received]
PHST- 2019/07/10 00:00 [accepted]
PHST- 2019/11/08 06:00 [entrez]
PHST- 2019/11/07 06:00 [pubmed]
PHST- 2019/11/07 06:01 [medline]
PHST- 2019/08/29 00:00 [pmc-release]
AID - 211700 [pii]
AID - 10.2147/DMSO.S211700 [doi]
PST - epublish
SO  - Diabetes Metab Syndr Obes. 2019 Aug 29;12:1645-1657. doi: 10.2147/DMSO.S211700. 
      eCollection 2019.