PMID- 31002154
OWN - NLM
STAT- MEDLINE
DCOM- 20200908
LR  - 20200908
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 23
IP  - 7
DP  - 2019 Apr
TI  - Influence of miR-34a on myocardial apoptosis in rats with acute myocardial 
      infarction through the ERK1/2 pathway.
PG  - 3034-3041
LID - 17585 [pii]
LID - 10.26355/eurrev_201904_17585 [doi]
AB  - OBJECTIVE: To study the influence of micro-ribonucleic acid (miR)-34a on 
      myocardial apoptosis in rats with acute myocardial infarction (AMI) through the 
      extracellular signal-regulated kinase 1/2 (ERK1/2) pathway. MATERIALS AND 
      METHODS: A total of 24 Sprague-Dawley (SD) rats were randomly divided into sham 
      group (n=12) and model group (n=12). The heart was exposed in the sham group, 
      while the AMI model was established in the model group. After sampling, the 
      morphology of myocardial tissues was observed via hematoxylin-eosin (HE) 
      staining, the expressions of B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X 
      protein (Bax) were detected via immunohistochemistry, and the protein expression 
      levels of ERK1/2 and phosphorylated ERK1/2 (p-ERK1/2) were detected via Western 
      blotting. Moreover, the expression of miR-34a was detected via quantitative 
      Polymerase Chain Reaction (qPCR), the apoptosis was detected via terminal 
      deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL), and the 
      myocardial injury indexes were detected using a fully-automatic biochemical 
      analyzer. RESULTS: The morphology of myocardial tissues was normal with a 
      complete structure in the sham group, while there was damage to myocardial 
      tissues in different degrees in the model group. The immunohistochemical results 
      revealed that the Bax expression was increased and the Bcl-2 expression was 
      decreased in the model group compared with those in the sham group (p<0.05). The 
      results of Western blotting showed that the protein expression levels of both 
      ERK1/2 and p-ERK1/2 were significantly increased in the model group compared with 
      those in the sham group (p<0.05). The qPCR results manifested that the expression 
      of miR-34a in the model group markedly declined compared with that in the sham 
      group (p<0.05). Besides, the TUNEL detection showed that the apoptosis rate in 
      the model group was remarkably increased compared with that in the sham group 
      (p<0.05), and the content of cardiac troponin T and creatine kinase isoenzyme in 
      the model group was significantly higher than that in the sham group ((p<0.05). 
      CONCLUSIONS: MiR-34a affects the apoptosis in AMI by regulating the ERK1/2 
      signaling pathway.
FAU - Bian, W-S
AU  - Bian WS
AD  - Department of Cardiovascular Medicine, Linyi No. 3 People's Hospital, Linyi, 
      China. gycq35@163.com.
FAU - Tian, F-H
AU  - Tian FH
FAU - Jiang, L-H
AU  - Jiang LH
FAU - Sun, Y-F
AU  - Sun YF
FAU - Wu, S-X
AU  - Wu SX
FAU - Gao, B-F
AU  - Gao BF
FAU - Kang, Z-X
AU  - Kang ZX
FAU - Zhuo, Z
AU  - Zhuo Z
FAU - Zhang, X-Z
AU  - Zhang XZ
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 (MIRN34 microRNA, rat)
RN  - 0 (MicroRNAs)
SB  - IM
MH  - Animals
MH  - Apoptosis/*physiology
MH  - MAP Kinase Signaling System/*physiology
MH  - Male
MH  - MicroRNAs/*biosynthesis/genetics
MH  - Myocardial Infarction/genetics/*metabolism/*pathology
MH  - Random Allocation
MH  - Rats
MH  - Rats, Sprague-Dawley
EDAT- 2019/04/20 06:00
MHDA- 2020/09/09 06:00
CRDT- 2019/04/20 06:00
PHST- 2019/04/20 06:00 [entrez]
PHST- 2019/04/20 06:00 [pubmed]
PHST- 2020/09/09 06:00 [medline]
AID - 17585 [pii]
AID - 10.26355/eurrev_201904_17585 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2019 Apr;23(7):3034-3041. doi: 
      10.26355/eurrev_201904_17585.