PMID- 31696494
OWN - NLM
STAT- MEDLINE
DCOM- 20201013
LR  - 20201013
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 23
IP  - 20
DP  - 2019 Oct
TI  - Effect of lncRNA MALAT1 on rats with myocardial infarction through regulating 
      ERK/MAPK signaling pathway.
PG  - 9041-9049
LID - 19306 [pii]
LID - 10.26355/eurrev_201910_19306 [doi]
AB  - OBJECTIVE: To explore the effect of the long non-coding ribonucleic acid (lncRNA) 
      metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on rats with 
      myocardial infarction (MI) by regulating the extracellular signal-regulated 
      kinase (ERK)/mitogen-activated protein kinase (MAPK) signaling pathway. MATERIALS 
      AND METHODS: The Sprague- Dawley (SD) rat model of MI was established, and lncRNA 
      MALAT1 was overexpressed using pcDNA-MALAT1 plasmids (MALAT1 group, n=10) and 
      silenced using RNA interference technique (siMALAT1 group, n=10). The Sham group 
      (n=10) was also set up. The transfection efficiency of lncRNA MALAT1 in rats was 
      detected via Reverse Transcription-Polymerase Chain Reaction (RT-PCR). 2 weeks 
      after the successful modeling, the cardiac function indexes were measured through 
      magnetic resonance imaging (MRI) and echocardiography (ECG). The myocardial 
      tissue injury was observed via hematoxylin-eosin (HE) staining, and the apoptosis 
      of myocardial tissues was detected via terminal deoxynucleotidyl 
      transferase-mediated dUTP nick end labeling (TUNEL) assay. Moreover, the levels 
      of the serum inflammatory factors were detected via enzyme-linked immunosorbent 
      assay (ELISA), the messenger RNA (mRNA) expressions of Collagen I and III, the 
      apoptosis, the and pathway genes were detected via RT-PCR. The expressions of 
      ERK/MAPK pathway-related proteins in myocardial tissues were detected via Western 
      blotting. RESULTS: The expression of lncRNA MALAT1 was remarkably increased in 
      the MALAT1 group but evidently declined in the siMALAT1 group (p<0.05), 
      indicating the successful transfection. The fractional shortening (FS, %) and 
      ejection fraction (EF, %) were significantly restored in siMALAT1 group (p<0.05), 
      suggesting that the silence of MALAT1 can improve the cardiac function after 
      acute MI. The results of the HE staining and TUNEL assay manifested that siMALAT1 
      group had milder myocardial injury and decreased apoptosis compared with MALAT1 
      group. In the MALAT1 group, the mRNA expressions of Collagen I and III, Caspase3, 
      ERK2, and MAPK were remarkably increased (p<0.05), while the mRNA expression of 
      Bcl-2 was remarkably decreased (p<0.05). The above expressions had the opposite 
      trends in siMALAT1 group. Besides, the protein expressions of ERK2 and MAPK in 
      MALAT1 group were significantly increased (p<0.05). CONCLUSIONS: The 
      downregulation of lncRNA MALAT1 can significantly improve the cardiac function 
      after MI in SD rats mainly by inhibiting the ERK/MAPK pathway.
FAU - Fan, Y-Z
AU  - Fan YZ
AD  - Department of Cardiology, Xiangtan Central Hospital, Xiangtan, China. 
      hh13607327390@126.com.
FAU - Huang, H
AU  - Huang H
FAU - Wang, S
AU  - Wang S
FAU - Tan, G-J
AU  - Tan GJ
FAU - Zhang, Q-Z
AU  - Zhang QZ
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 (MALAT1 long noncoding RNA, rat)
RN  - 0 (RNA, Long Noncoding)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Disease Models, Animal
MH  - *MAP Kinase Signaling System
MH  - Male
MH  - Myocardial Infarction/*genetics/metabolism
MH  - RNA, Long Noncoding/*genetics
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Signal Transduction
MH  - *Up-Regulation
EDAT- 2019/11/07 06:00
MHDA- 2020/10/21 06:00
CRDT- 2019/11/08 06:00
PHST- 2019/11/08 06:00 [entrez]
PHST- 2019/11/07 06:00 [pubmed]
PHST- 2020/10/21 06:00 [medline]
AID - 19306 [pii]
AID - 10.26355/eurrev_201910_19306 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2019 Oct;23(20):9041-9049. doi: 
      10.26355/eurrev_201910_19306.