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.
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.
Authors: Changjun Luo; Si Xiong; Yiteng Huang; Ming Deng; Jing Zhang; Jianlin Chen; Rongfeng Yang; Xiao Ke Journal: Front Cell Dev Biol Date: 2021-07-12