PMID- 30402863
OWN - NLM
STAT- MEDLINE
DCOM- 20191112
LR  - 20210331
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 22
IP  - 20
DP  - 2018 Oct
TI  - Suppression of microRNA-101 attenuates hypoxia-induced myocardial H9c2 cell 
      injury by targeting DIMT1-Sp1/survivin pathway.
PG  - 6965-6976
LID - 16167 [pii]
LID - 10.26355/eurrev_201810_16167 [doi]
AB  - OBJECTIVE: MicroRNAs (miRNAs) are small single-stranded RNAs in eukaryotic cells, 
      which play important regulatory roles in the pathogenesis of various diseases. We 
      aimed to investigate the effects of miRNA-101 (miR-101) on hypoxia-induced 
      myocardial infarction (MI) cell injury model (myocardial H9c2 cell injury model). 
      The possible target gene of miR-101 was also analyzed. MATERIALS AND METHODS: 
      H9c2 cells were exposed to hypoxia treatment. Cell viability, migration, 
      invasion, apoptosis and the expression of miR-101 were detected using CCK-8 
      assay, transwell assay, flow cytometer analysis, Western blotting and qRT-PCR, 
      respectively. Then, the effects of miR-101 overexpression or suppression on the 
      cell injury induced by hypoxia were assessed. Dual luciferase reporter assay was 
      used to analyze the possible target gene of miR-101. Finally, the effects of 
      dimethyladenosine transferase 1 homolog (DIMT1), the possible target gene of 
      miR-101, on H9c2 cell injury were investigated. RESULTS: Hypoxia significantly 
      induced H9c2 cell injury. miR-101 was up-regulated after hypoxia induction. 
      Hypoxia-induced cell injury was significantly reversed by miR-101 suppression and 
      exacerbated by miR-101 overexpression. DIMT1 was a direct target gene of miR-101. 
      Knockdown of DIMT1 markedly inhibited the protective effects of miR-101 
      suppression on hypoxia-induced cell injury by suppressing specific protein 1 
      (Sp1)/Survivin pathway. CONCLUSIONS: We verified the critical roles of miR-101 in 
      regulating myocardial cell injury induced by hypoxia. DIMT1-mediated the 
      Sp1/Survivin pathway was also involved in this process. Our findings replenished 
      the understanding of the regulatory roles of miRNAs in hypoxia-induced MI cell 
      injury and provided new molecular target for therapy and diagnosis of MI.
FAU - Guo, Z-X
AU  - Guo ZX
AD  - Department of Cardiology, Taian City Central Hospital, Taian, China. 
      zhanghuanyi0011@126.com.
FAU - Zhou, F-Z
AU  - Zhou FZ
FAU - Song, W
AU  - Song W
FAU - Yu, L-L
AU  - Yu LL
FAU - Yan, W-J
AU  - Yan WJ
FAU - Yin, L-H
AU  - Yin LH
FAU - Sang, H
AU  - Sang H
FAU - Zhang, H-Y
AU  - Zhang HY
LA  - eng
PT  - Journal Article
PT  - Retracted Publication
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 0 (MIRN101 microRNA, rat)
RN  - 0 (MicroRNAs)
RN  - 0 (Sp1 Transcription Factor)
RN  - 0 (Survivin)
RN  - EC 2.- (Transferases)
SB  - IM
RIN - Eur Rev Med Pharmacol Sci. 2020 Dec;24(23):11986. PMID: 33336713
MH  - Animals
MH  - Apoptosis/genetics
MH  - Cell Hypoxia/*genetics
MH  - Cell Line
MH  - Cell Survival/genetics
MH  - Hypoxia/metabolism
MH  - MicroRNAs/*genetics
MH  - Myocytes, Cardiac/metabolism
MH  - Rats
MH  - Signal Transduction
MH  - Sp1 Transcription Factor/*metabolism
MH  - Survivin/*metabolism
MH  - Transferases/genetics
MH  - Up-Regulation
EDAT- 2018/11/08 06:00
MHDA- 2019/11/13 06:00
CRDT- 2018/11/08 06:00
PHST- 2018/11/08 06:00 [entrez]
PHST- 2018/11/08 06:00 [pubmed]
PHST- 2019/11/13 06:00 [medline]
AID - 16167 [pii]
AID - 10.26355/eurrev_201810_16167 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2018 Oct;22(20):6965-6976. doi: 
      10.26355/eurrev_201810_16167.