PMID- 31298394
OWN - NLM
STAT- MEDLINE
DCOM- 20201001
LR  - 20201001
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 23
IP  - 12
DP  - 2019 Jun
TI  - MicroRNA-361 regulates apoptosis of cardiomyocytes after ischemic-reperfusion 
      injury.
PG  - 5413-5421
LID - 18210 [pii]
LID - 10.26355/eurrev_201906_18210 [doi]
AB  - OBJECTIVE: To investigate the role and mechanism of microRNA-361 (miR-361) in 
      apoptosis after myocardial ischemia-reperfusion (MI-R) injury. MATERIALS AND 
      METHODS: For the in vivo experiments, the mice model of MI-R injury was 
      established, and miR-361 was up-regulated via lentivirus with miR-298 
      overexpression. The expression of miR-361 and Bcl-2 associated X protein (BAX) 
      were detected via Real Time-quantitative Polymerase Chain Reaction (qPCR) and 
      Western blot (WB), respectively. Terminal deoxynucleotidyl transferase-mediated 
      dUTP nick end labeling (TUNEL) assay was used to detect the apoptosis in 
      myocardial tissues. MI-R injury was also simulated in vitro experiments, and the 
      relationship between miR-361 and BAX was verified using Luciferase reporter 
      vector. The effect of miR-361 on cardiomyocyte apoptosis was also detected at the 
      cellular level. RESULTS: In vivo experiments showed that the miR-361 expression 
      was down-regulated at MI-R injury area. The up-regulation of miR-361 
      significantly decreased the expression of BAX, reduced the myocardial apoptosis 
      and inhibited the mitochondrial apoptosis pathway protein expression, including 
      the cytochrome-c (Cyt-C) and cleaved caspase-3. In vitro experiments revealed 
      that BAX was a target gene of miR-361 and further proved that miR-361 could 
      inhibit the cytochrome-c and cleaved caspase-3 expression, as well as reduce the 
      myocardial apoptosis through BAX. CONCLUSIONS: MiR-361 could improve the 
      myocardial apoptosis through the target gene BAX in MI-R injury.
FAU - Xie, Y
AU  - Xie Y
AD  - Intensive Care Unit, Maternity and Child Health Care of Zaozhuang, Zaozhuang, 
      China. 18906322555@189.cn.
FAU - Yao, F-L
AU  - Yao FL
FAU - Li, X
AU  - Li X
LA  - eng
PT  - Journal Article
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 0 (Bax protein, mouse)
RN  - 0 (MIRN361 microRNA, mouse)
RN  - 0 (MicroRNAs)
RN  - 0 (bcl-2-Associated X Protein)
RN  - 9007-43-6 (Cytochromes c)
RN  - EC 3.4.22.- (Casp3 protein, mouse)
RN  - EC 3.4.22.- (Caspase 3)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Apoptosis/*genetics
MH  - Caspase 3/metabolism
MH  - Cells, Cultured
MH  - Cytochromes c/metabolism
MH  - Disease Models, Animal
MH  - Down-Regulation
MH  - Humans
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - MicroRNAs/*metabolism
MH  - Myocardial Reperfusion Injury/*pathology
MH  - Myocardium/cytology/*pathology
MH  - Myocytes, Cardiac/pathology
MH  - Primary Cell Culture
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Signal Transduction/genetics
MH  - Up-Regulation
MH  - bcl-2-Associated X Protein/*genetics/metabolism
EDAT- 2019/07/13 06:00
MHDA- 2020/10/02 06:00
CRDT- 2019/07/13 06:00
PHST- 2019/07/13 06:00 [entrez]
PHST- 2019/07/13 06:00 [pubmed]
PHST- 2020/10/02 06:00 [medline]
AID - 18210 [pii]
AID - 10.26355/eurrev_201906_18210 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2019 Jun;23(12):5413-5421. doi: 
      10.26355/eurrev_201906_18210.