Abstract
Numerous studies have shown that long noncoding RNAs (lncRNAs) play essential roles in the development and progression of human cardiovascular diseases. However, whether lncRNA ezrin antisense RNA 1 (EZR-AS1) is associated with the progression of coronary heart disease (CHD) remains unclear. Accordingly, the aim of the present study was to evaluate the role of lncRNA EZR-AS1 in patients with CHD and in human venous endothelial cells (HUVECs). The findings revealed that lncRNA EZR-AS1 was highly expressed in the peripheral blood of patients with CHD. In vitro experiments showed that the overexpression of EZR-AS1 could enhance proliferation, migration, and apoptosis by upregulating the expression of EZR in HUVECs; downregulation of lncRNA EZR-AS1 resulted in the opposite effect. lncRNA EZR-AS1 was also found to regulate SET and MYND domain-containing protein 3 (SMYD3), a histone H3 lysine 4-specific methyltransferase, which subsequently mediated EZR transcription. Collectively, these results demonstrate that lncRNA EZR-AS1 plays an important role in HUVECs function via SMYD3 signaling.
Highlights
As a result of economic development and an aging population, the risk of developing cardiovascular disease has gradually increased [1, 2]
The results revealed that ezrin antisense RNA 1 (EZR-AS1) expression was markedly upregulated in patients with Coronary heart disease (CHD), compared with the controls (Figure 1(a))
RT-qPCR was used to analyze the expression of EZR-AS1 in the peripheral blood of patients with severe CHD and controls
Summary
As a result of economic development and an aging population, the risk of developing cardiovascular disease has gradually increased [1, 2]. Recent studies have shown that lncRNAs are involved in the development and progression of various cardiovascular diseases [7,8,9,10,11], including heart failure, myocardial hypertrophy, heart metabolic disease, myocardial infarction, and atherosclerosis (AS). Ezrin (EZR) is a member of the ezrin-radixin-moesin (ERM) family of cytoskeletal proteins, which connects the actin cytoskeleton to the plasma membrane. SET and MYND domain-containing protein 3 (SMYD3) is a member of the SET and MYND domain (SMYD) family. Studies have shown that SMYD3 interacts with the specific region of trimethylation of histone H3 lysine 4- (H3K4Me3-) modified histone tails, which contributes its recruitment to the key promoter regions of downstream genes and activates the gene expression [14, 15].
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