ArticleImmunity, inflammation and disease2023
By modulating miR-525-5p/Bax axis, LINC00659 promotes vascular endothelial cell apoptosis.
Article in Immunity, inflammation and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- The Role of Circulating MicroRNAs as Biomarkers and Therapeutic Targets in Venous Thromboembolism: A Systematic Review.Journal of clinical medicine · 2026Review
- LncRNA MAGI2-AS3 promotes the progression of atherosclerosis by sponging miR-525-5p.Journal of cardiothoracic surgery · 2025Article
- Curdione protects vascular endothelial cells and atherosclerosis via the regulation of DNMT1-mediated ERBB4 promoter methylation.Open medicine (Warsaw, Poland) · 2025Article
- Macrophage Tim-4 protects against deep vein thrombosis by binding CK2β to suppress inflammatory responses.Frontiers in immunology · 2025Article
- Long Non-Coding RNAs in Venous Thromboembolism: Where Do We Stand?International journal of molecular sciences · 2023Review
- By modulating miR-525-5p/Bax axis, LINC00659 promotes vascular endothelial cell apoptosis.Immunity, inflammation and disease · 2023Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDeep vein thrombosis (DVT) is a vascular disease that has no effective treatment at present. Endothelial cells play a crucial role in the processes vasoconstriction, platelet activation, and blood coagulation and are an integral part of the vascular response to injury resulting in thrombus formation.
objectiveThe aim of this study was to investigate the roles and mechanisms of long noncoding RNA LINC00659 (LINC00659) in endothelial cells.
methodsThe functions of LINC00659 and miR-525-5p on endothelial cells were explored by cell transfection assays, and the expression levels of LINC00659, miR-525-5p, and Bax in human umbilical vein endothelial cells (HUVECs) were assessed with reverse transcriptase-quantitative polymerase chain reaction (RT-qPCR). Binding sites of LINC00659 and miR-525-5p were subsequently analyzed with bioinformatics software, and validated with dual-luciferase reporter gene assay. Effects of LINC00659 and miR-525-5p on proliferation and apoptosis of HUVECs were detected with MTT (3-(45)-dimethylthiahiazo (-z-y1)-35-di-phenytetrazoliumromide) assay and flow cytometry. RT-qPCR and western blot analysis were used to evaluate the mRNA and protein levels of apoptosis-related markers Bcl-2 and Bax in HUVECs.
resultsLINC00659 directly targeted and negatively regulated miR-525-5p, and Bax was a target of miR-525-5p. Upregulation of LINC00659 could inhibit proliferation and promote apoptosis of HUVECs, while the silencing of LINC00659 could increase the viability of HUVECs and inhibit apoptosis via upregulating miR-525-5p. Further mechanistic studies revealed miR-525-5p could negatively regulate Bax in HUVECs, and increased the viability of HUVECs and inhibited apoptosis by downregulating Bax expression.
conclusionLINC00659 played an important role in DVT by regulating the apoptosis of vascular endothelial cells through regulating miR-525-5p/Bax axis.
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