PMID- 31364134
OWN - NLM
STAT- MEDLINE
DCOM- 20200930
LR  - 20200930
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 23
IP  - 14
DP  - 2019 Jul
TI  - MiR-181a affects myocardial ischemia-reperfusion injury in rats via regulating 
      akt signaling pathway.
PG  - 6292-6298
LID - 18451 [pii]
LID - 10.26355/eurrev_201907_18451 [doi]
AB  - OBJECTIVE: The aim of this study was to explore the influence of the micro 
      ribonucleic acid (miR)-181a on myocardial ischemia-reperfusion injury (MIRI) in 
      rats by regulating the protein kinase B (Akt) signaling pathway. MATERIALS AND 
      METHODS: A total of 30 male Sprague-Dawley rats were randomly divided into three 
      groups, including: sham operation group (Sham group), ischemia-reperfusion group 
      (I/R group), and miR group (MiR-181a group). The model of myocardial 
      ischemia-reperfusion was successfully established in rats. The concentration of 
      blood nitric oxide (NO) was detected by the relative kits. Myocardial apoptosis 
      in rats of the three groups was detected using terminal deoxynucleotidyl 
      transferase-mediated dUTP nick end labeling (TUNEL) assay. Furthermore, the 
      expressions of myocardial cell apoptosis-related proteins and tumor necrosis 
      factor-alpha (TNF-alpha), and the degree of Akt phosphorylation were determined by 
      Western blotting. RESULTS: Compared with Sham group and miR-181a group, I/R group 
      exhibited significantly elevated left ventricular end-diastolic pressure (LVEDP) 
      (p<0.05). However, the left ventricular end-systolic pressure (LVESP), stroke 
      work (SW), differential pressure (DP), end-systolic pressure-volume relationship 
      (ESPVR), and end-diastolic pressure-volume relationship (EDPVR) significantly 
      decreased in the I/R group (p<0.05). In comparison with miR-181a group, the 
      apoptosis index of myocardial cells was remarkably elevated in the I/R group, 
      showing statistically significant differences (p<0.05). The protein bands were 
      analyzed using the Quantity One detection software. The results demonstrated 
      that, compared with the Sham group, I/R group showed significantly elevated 
      expressions of cysteine-aspartic protease (Caspase)-3 and TNF-alpha in rat myocardial 
      tissues (p<0.05). However, the protein levels of Akt and endothelial NO synthase 
      (eNOS) phosphorylation and NO in rat myocardial cells were significantly 
      down-regulated (p<0.05). CONCLUSIONS: MiR-181a activates Akt to promote the 
      phosphorylation of its downstream protein eNOS, inhibit the apoptosis of 
      myocardial cells, and alleviate MIRI.
FAU - Zhang, L-X
AU  - Zhang LX
AD  - Department of Gerontology, The Third Hospital of Hebei Medical University, 
      Shijiazhuang, China. daylight1981@126.com.
FAU - Ding, F
AU  - Ding F
FAU - Wang, C-Q
AU  - Wang CQ
FAU - Bing, Q
AU  - Bing Q
FAU - Zhao, Z
AU  - Zhao Z
FAU - Wang, J
AU  - Wang J
FAU - Zhang, L
AU  - Zhang L
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 (MIRN181 microRNA, rat)
RN  - 0 (MicroRNAs)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type III)
RN  - EC 1.14.13.39 (Nos3 protein, rat)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
SB  - IM
MH  - Animals
MH  - Disease Models, Animal
MH  - Heart Function Tests
MH  - Male
MH  - MicroRNAs/*genetics
MH  - Myocardial Reperfusion Injury/*genetics/metabolism/physiopathology
MH  - Nitric Oxide Synthase Type III/metabolism
MH  - Phosphorylation
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Random Allocation
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - *Signal Transduction
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2019/08/01 06:00
MHDA- 2020/10/02 06:00
CRDT- 2019/08/01 06:00
PHST- 2019/08/01 06:00 [entrez]
PHST- 2019/08/01 06:00 [pubmed]
PHST- 2020/10/02 06:00 [medline]
AID - 18451 [pii]
AID - 10.26355/eurrev_201907_18451 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2019 Jul;23(14):6292-6298. doi: 
      10.26355/eurrev_201907_18451.