PMID- 31217870
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200929
IS  - 1943-8141 (Print)
IS  - 1943-8141 (Electronic)
IS  - 1943-8141 (Linking)
VI  - 11
IP  - 5
DP  - 2019
TI  - MiR-21b-3p protects NS2OY cells against oxygen-glucose 
      deprivation/reperfusion-induced injury by down-regulating cyclooxygenase-2.
PG  - 3007-3017
AB  - Recent studies have shown abnormal expression levels of cyclooxygenase-2 (COX-2) 
      and miR-21b-3p in cerebral ischemia-reperfusion (I/R) rat models. Decreased COX-2 
      expression could reduce brain injury and thus could be a target of miR-21b-3p 
      according to the miRNA databases (miRDB) analysis. However, its functions and 
      underlying mechanisms in I/R injury remain unclear. In our study, we have 
      established an oxygen/glucose deprivation and reperfusion (OGD/R) model by using 
      NS2OY cells. The expression of miR-21b-3p and COX-2 was determined by 
      quantitative real-time PCR or Western blot, and the fluorescence intensities were 
      detected by fluorescence in situ hybridization (FISH) or immunofluorescence. 
      After transfection and OGD/R treatments, the functions of miR-21b-3p and COX-2 on 
      cell viability and apoptosis were detected using cell-counting kit 8, Edu 
      staining, flow cytometry and Hoechst staining, respectively. Finally, 
      dual-luciferase reporter assay was used to explore the relationship between 
      miR-21-b-3p and COX-2. The results have showed that COX-2 mRNA and protein 
      expression were significantly increased; however, the expression of miR-21b-3p 
      was remarkably reduced in NS2OY cells after OGD/R treatment. The changes were 
      most remarkable in OGD 2 h/R24 group. Function analysis has showed that when 
      NS2OY cells were exposed to OGD/R injury, overexpressed miR-21b-3p significantly 
      downregulated COX-2 expression, increased cell viability and decreased apoptosis. 
      In addition, knocking down the expression of COX-2 could also increase cell 
      viability and decrease apoptosis. Dual-luciferase reporter assays showed 
      miR-21b-3p as the target of 3'-UTR of COX-2. Therefore, we concluded that 
      OGD/R-induced injury by down-regulating COX-2.
FAU - Wu, Xiaona
AU  - Wu X
AD  - Department of Neurology, General Hospital of Southern Theater Command, PLA 
      Guangzhou, Guangdong, People's Republic of China.
FAU - Peng, Kairun
AU  - Peng K
AD  - Department of Neurology, General Hospital of Southern Theater Command, PLA 
      Guangzhou, Guangdong, People's Republic of China.
FAU - Huang, Huai
AU  - Huang H
AD  - Department Two of Nerve Rehabilitation, Guangzhou General Hospital, Guangzhou 
      Military Region Guangzhou, Guangdong, People's Republic of China.
FAU - Li, Zhensheng
AU  - Li Z
AD  - Department of Neurology, General Hospital of Southern Theater Command, PLA 
      Guangzhou, Guangdong, People's Republic of China.
FAU - Xiang, Wei
AU  - Xiang W
AD  - Department of Neurology, General Hospital of Southern Theater Command, PLA 
      Guangzhou, Guangdong, People's Republic of China.
FAU - Deng, Wenting
AU  - Deng W
AD  - Department of Neurology, General Hospital of Southern Theater Command, PLA 
      Guangzhou, Guangdong, People's Republic of China.
FAU - Liu, Liu
AU  - Liu L
AD  - Department of Neurology, General Hospital of Southern Theater Command, PLA 
      Guangzhou, Guangdong, People's Republic of China.
FAU - Li, Wei
AU  - Li W
AD  - General Hospital of Northern Theater Command, PLA Shenyang, Liaoning, People's 
      Republic of China.
FAU - Zhang, Tao
AU  - Zhang T
AD  - Department of Orthopaedics, General Hospital of Southern Theater Command, PLA 
      Guangzhou, Guangdong, People's Republic of China.
LA  - eng
PT  - Journal Article
DEP - 20190515
PL  - United States
TA  - Am J Transl Res
JT  - American journal of translational research
JID - 101493030
PMC - PMC6556624
OTO - NOTNLM
OT  - Oxygen/glucose deprivation and reperfusion
OT  - apoptosis
OT  - cell viability
OT  - cyclooxygenase-2
OT  - miR-21b-3p
COIS- None.
EDAT- 2019/06/21 06:00
MHDA- 2019/06/21 06:01
PMCR- 2019/05/15
CRDT- 2019/06/21 06:00
PHST- 2018/07/13 00:00 [received]
PHST- 2018/12/23 00:00 [accepted]
PHST- 2019/06/21 06:00 [entrez]
PHST- 2019/06/21 06:00 [pubmed]
PHST- 2019/06/21 06:01 [medline]
PHST- 2019/05/15 00:00 [pmc-release]
PST - epublish
SO  - Am J Transl Res. 2019 May 15;11(5):3007-3017. eCollection 2019.