PMID- 29990866
OWN - NLM
STAT- MEDLINE
DCOM- 20181218
LR  - 20181218
IS  - 1950-6007 (Electronic)
IS  - 0753-3322 (Linking)
VI  - 106
DP  - 2018 Oct
TI  - Knockdown of lncRNA MALAT1 attenuates acute myocardial infarction through 
      miR-320-Pten axis.
PG  - 738-746
LID - S0753-3322(18)33482-6 [pii]
LID - 10.1016/j.biopha.2018.06.122 [doi]
AB  - BACKGROUND: Long noncoding RNA (LncRNA) metastasis-associated lung adenocarcinoma 
      transcript 1 (MALAT1) is involved in the development of acute myocardial 
      infarction (AMI). However, the molecular mechanism and biological function of 
      MALAT1 in AMI remained unclear. METHODS: The expression levels of MALAT1, miR-320 
      and phosphatase and tensin homolog deleted on chromosome 10 (Pten) in a mouse 
      model of AMI and sham-operated mice were determined by quantitative real-time PCR 
      (qRT-PCR) and western blotting, respectively. The relationships between miR-320 
      and MALAT1, Pten were confirmed by luciferase reporter assay. The roles of 
      MALAT1, miR-320 and Pten in myocardial apoptosis were evaluated using Annexin 
      V-FITC/PI double-labeled flow cytometry. Echocardiographic evaluation, serum 
      creatine kinase MB (CK-MB) and lactate dehydrogenase (LDH), myocardial infarct 
      size and myocardial apoptosis using terminal dexynucleotidyl transferase-mediated 
      dUTP nick end labeling (TUNEL) assay were used to examine the impact of MALAT1 on 
      myocardial injury. RESULTS: MALAT1 and Pten were highly expressed, while miR-320 
      was suppressed in MI group. Mechanistically, MALAT1 may serve as a sponge for 
      miR-320 to upregulate Pten, a direct target of miR-320. Moreover, MALAT1 
      knockdown overturned the pro-apoptotic effect of miR-320 in vitro and in vivo. 
      CONCLUSION: MALAT1 knockdown attenuated myocardial apoptosis through suppressing 
      Pten expression by sponging miR-320 in mouse AMI.
CI  - Copyright (c) 2018. Published by Elsevier Masson SAS.
FAU - Hu, Hao
AU  - Hu H
AD  - Department of Cardiovascular, The First Affiliated Hospital of USTC, Hefei 
      230001, Anhui, China; Division of Life Sciences and Medicine, University of 
      Science and Technology of China, Hefei 230001, Anhui, China.
FAU - Wu, Jiawei
AU  - Wu J
AD  - Department of Cardiovascular, The First Affiliated Hospital of USTC, Hefei 
      230001, Anhui, China; Division of Life Sciences and Medicine, University of 
      Science and Technology of China, Hefei 230001, Anhui, China.
FAU - Li, Dan
AU  - Li D
AD  - Department of Cardiovascular, The First Affiliated Hospital of USTC, Hefei 
      230001, Anhui, China; Division of Life Sciences and Medicine, University of 
      Science and Technology of China, Hefei 230001, Anhui, China.
FAU - Zhou, Junling
AU  - Zhou J
AD  - Department of Cardiovascular, The First Affiliated Hospital of USTC, Hefei 
      230001, Anhui, China; Division of Life Sciences and Medicine, University of 
      Science and Technology of China, Hefei 230001, Anhui, China.
FAU - Yu, Hua
AU  - Yu H
AD  - Department of Cardiovascular, The First Affiliated Hospital of USTC, Hefei 
      230001, Anhui, China; Division of Life Sciences and Medicine, University of 
      Science and Technology of China, Hefei 230001, Anhui, China.
FAU - Ma, Likun
AU  - Ma L
AD  - Department of Cardiovascular, The First Affiliated Hospital of USTC, Hefei 
      230001, Anhui, China; Division of Life Sciences and Medicine, University of 
      Science and Technology of China, Hefei 230001, Anhui, China. Electronic address: 
      likunma633@yeah.net.
LA  - eng
PT  - Journal Article
DEP - 20180711
PL  - France
TA  - Biomed Pharmacother
JT  - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
JID - 8213295
RN  - 0 (Malat1 long non-coding RNA, mouse)
RN  - 0 (MicroRNAs)
RN  - 0 (Mirn320 microRNA, mouse)
RN  - 0 (RNA, Long Noncoding)
RN  - EC 3.1.3.67 (PTEN Phosphohydrolase)
RN  - EC 3.1.3.67 (Pten protein, mouse)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Cells, Cultured
MH  - Disease Models, Animal
MH  - Gene Expression Regulation, Enzymologic
MH  - *Gene Knockdown Techniques
MH  - Male
MH  - Mice, Inbred C57BL
MH  - MicroRNAs/genetics/*metabolism
MH  - Myocardial Infarction/*enzymology/*genetics/pathology/physiopathology
MH  - Myocardium/*enzymology/pathology
MH  - PTEN Phosphohydrolase/genetics/*metabolism
MH  - *RNA Interference
MH  - RNA, Long Noncoding/*genetics/metabolism
MH  - Signal Transduction
MH  - Stroke Volume
MH  - Time Factors
MH  - Ventricular Function, Left
MH  - Ventricular Pressure
OTO - NOTNLM
OT  - Apoptosis
OT  - MALAT1
OT  - Myocardial infarction
OT  - Pten
OT  - miR-320
EDAT- 2018/07/11 06:00
MHDA- 2018/12/19 06:00
CRDT- 2018/07/11 06:00
PHST- 2018/05/23 00:00 [received]
PHST- 2018/06/20 00:00 [revised]
PHST- 2018/06/21 00:00 [accepted]
PHST- 2018/07/11 06:00 [pubmed]
PHST- 2018/12/19 06:00 [medline]
PHST- 2018/07/11 06:00 [entrez]
AID - S0753-3322(18)33482-6 [pii]
AID - 10.1016/j.biopha.2018.06.122 [doi]
PST - ppublish
SO  - Biomed Pharmacother. 2018 Oct;106:738-746. doi: 10.1016/j.biopha.2018.06.122. 
      Epub 2018 Jul 11.