PMID- 31486508
OWN - NLM
STAT- MEDLINE
DCOM- 20201207
LR  - 20201214
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 23
IP  - 16
DP  - 2019 Aug
TI  - MiR-34a promotes myocardial infarction in rats by inhibiting the activity of 
      SIRT1.
PG  - 7059-7065
LID - 18750 [pii]
LID - 10.26355/eurrev_201908_18750 [doi]
AB  - OBJECTIVE: To investigate the effect of micro ribonucleic acid (miR)-34a 
      regulating silent information regulator 1 (SIRT1) on myocardial infarction (MI) 
      rats. MATERIALS AND METHODS: A total of 30 male, 8-week-old rats were divided 
      into three groups, including: sham group (M group), MI group and MI + miR-34a 
      treatment group (miR group). Tissue morphology in the MI region was observed via 
      hematoxylin-eosin (HE) staining. Myocardial apoptosis in the three groups was 
      detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end 
      labeling (TUNEL) assay. Furthermore, the protein levels of SIRT1, B-cell 
      lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax) in myocardial cells were 
      detected via Western blotting. RESULTS: Compared with M group, left ventricular 
      end-diastolic diameter (LVEDD) and left ventricular end-systolic diameter (LVESD) 
      increased significantly in MI group and miR group (p<0.05), while left 
      ventricular ejection fraction (LVEF) and fractional shortening (FS) decreased 
      obviously (p<0.05). The results of HE staining showed that the inflammatory 
      infiltration of myocardial cells and intercellular collagen fibers significantly 
      increased, and the neuronal damage was remarkably aggravated in MI group and miR 
      group when compared with M group (p<0.05). Compared with MI group, myocardial 
      necrosis, inflammatory cell infiltration and intercellular collagen fibers all 
      increased significantly in miR group (p<0.05). Moreover, the results of TUNEL 
      assay revealed that myocardial apoptosis rate in MI group [(21.35+/-3.12)%] was 
      remarkably higher than that of M group [(9.53+/-1.17)%]. Meanwhile, it was 
      significantly higher in miR group [(42.38+/-3.44)%)] than that of MI group, 
      displaying statistically significant differences (p<0.05). The number of 
      apoptotic cells increased obviously in MI group when compared with M group, while 
      it decreased significantly in MI group when compared with miR group (p<0.05). 
      Besides, the protein levels of SIRT1 and Bcl-2 in myocardial tissues in miR group 
      were remarkably lower than those of M group and MI group (p<0.05). Furthermore, 
      the protein level of Bax in miR group was higher than that of M group and MI 
      group, and there were statistically significant differences (p<0.05). 
      CONCLUSIONS: Overexpression of miR-34a inhibits the activity of SIRT1, thereby 
      promoting the apoptosis of MI.
FAU - Dong, F-F
AU  - Dong FF
AD  - Department of Cardiology, Changhai Hospital, Shanghai, China. zhaoxx1112@126.com.
FAU - Dong, S-H
AU  - Dong SH
FAU - Liang, Y
AU  - Liang Y
FAU - Wang, K
AU  - Wang K
FAU - Qin, Y-W
AU  - Qin YW
FAU - Zhao, X-X
AU  - Zhao XX
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)
RN  - EC 3.5.1.- (Sirt1 protein, rat)
RN  - EC 3.5.1.- (Sirtuin 1)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Disease Models, Animal
MH  - Male
MH  - MicroRNAs/*metabolism
MH  - Myocardial Infarction/diagnosis/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sirtuin 1/*antagonists & inhibitors/metabolism
EDAT- 2019/09/06 06:00
MHDA- 2020/12/15 06:00
CRDT- 2019/09/06 06:00
PHST- 2019/09/06 06:00 [entrez]
PHST- 2019/09/06 06:00 [pubmed]
PHST- 2020/12/15 06:00 [medline]
AID - 18750 [pii]
AID - 10.26355/eurrev_201908_18750 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2019 Aug;23(16):7059-7065. doi: 
      10.26355/eurrev_201908_18750.