ArticleCell cycle (Georgetown, Tex.)2022
Long non-coding RNA MCM3AP antisense RNA 1 silencing upregulates microRNA-24-3p to accelerate proliferation and migration of vascular endothelial cells in myocardial infarction rats by reducing EIF4G2.
Article in Cell cycle (Georgetown, Tex.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 8 citations in OpenAlex.
- CASC15 participated in the damage of vascular endothelial cells in atherosclerosis through interaction with miR-940.BMC medical genomics · 2025Article
- Importance of long non-coding RNAs in the pathogenesis, diagnosis, and treatment of myocardial infarction.International journal of cardiology. Heart & vasculature · 2024Review
- Diagnostic and Predictive Value of LncRNA MCM3AP-AS1 in Sepsis and Its Regulatory Role in Sepsis-Induced Myocardial Dysfunction.Cardiovascular toxicology · 2024Article
- Comparative Analysis of Transcriptome Profiles in Patients with Thromboangiitis Obliterans.Genes · 2023Article
- Noncoding RNAs as Key Regulators for Cardiac Development and Cardiovascular Diseases.Journal of cardiovascular development and disease · 2023Review
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Authors and funding
7 authors at 1 institution in 1 country.
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Abstract
Long non-coding RNAs (lncRNAs) are crucial drivers in the progression of human diseases such as myocardial infarction (MI). However, the impact of lncRNA MCM3AP antisense RNA 1 (MCM3AP-AS1) on MI remains unknown. This research was determined to explore the effect of MCM3AP-AS1 modulating microRNA-24-3p (miR-24-3p) and eukaryotic translation initiation factor 4 gamma 2 (EIF4G2) on MI. The rat MI models were constructed and, respectively, treated with altered MCM3AP-AS1, miR-24-3p or/and EIF4G2. Subsequently, the cardiac function, myocardial pathological injury, malondialdehyde content and superoxide dismutase activity were determined. The vascular endothelial cells (VECs) were isolated and treated severally, and then proliferation and migration of VECs were measured. MCM3AP-AS1, miR-24-3p, EIF4G2 and vascular endothelial growth factor (VEGF) expressions in myocardial tissues and VECs were assessed. MCM3AP-AS1 and EIF4G2 were upregulated while miR-24-3p and VEGF were downregulated in MI rat myocardial tissues. MCM3AP-AS1 silencing or miR-24-3p elevation improved cardiac function and myocardial pathological injury, suppressed malondialdehyde content, and also enhanced VEGF expression and superoxide dismutase activity in MI rats. In VECs, downregulated MCM3AP-AS1 or upregulated miR-24-3p accelerated cell proliferation and migration. These effects of miR-24-3p upregulation were reversed by overexpressed EIF4G2. Our study summarizes that reduced MCM3AP-AS1 elevates miR-24-3p to promote proliferation and migration of MI rat VECs by inhibiting EIF4G2.
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