ArticleFrontiers in molecular biosciences2021
Long Non-Coding RNA MEG8 Suppresses Hypoxia-Induced Excessive Proliferation, Migration and Inflammation of Vascular Smooth Muscle Cells by Regulation of the miR-195-5p/RECK Axis.
Article in Frontiers in molecular biosciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Tiaozhi Tongmai Formula attenuates atherosclerosis by modulating the JAK1/STAT3 pathway to inhibit phenotypic transformation of vascular smooth muscle cells.Cardiovascular diagnosis and therapy · 2026Article
- LncRNA MEG8 promotes deep vein thrombosis by sponging miR-296-5p to regulate human umbilical vein endothelial cells.Hereditas · 2025Article
- RECK as a Potential Crucial Molecule for the Targeted Treatment of Sepsis.Journal of inflammation research · 2025Review
- Machine Learning-Based Prediction of Post-Operative Systemic Inflammatory Response Syndrome Following Pediatric Percutaneous Nephrolithotripsy.Journal of inflammation research · 2025Article
- Mutated LRRK2 induces a reactive phenotype and alters migration in human iPSC-derived pericyte-like cells.Fluids and barriers of the CNS · 2024Article
- LncRNA MEG8 ameliorates Parkinson's disease neuro-inflammation through miR-485-3p/FBXO45 axis.Acta neurologica Belgica · 2024Article
- The role of splicing events in the inflammatory response of atherosclerosis: molecular mechanisms and modulation.Frontiers in immunology · 2024Review
- Recent Updates on the Therapeutic Prospects of Reversion-Inducing Cysteine-Rich Protein with Kazal Motifs (RECK) in Liver Injuries.International journal of molecular sciences · 2023Review
- Long non‑coding RNAExperimental and therapeutic medicine · 2023Article
- Long non-coding RNA HIF1A-AS2 modulates the proliferation, migration, and phenotypic switch of aortic smooth muscle cells in aortic dissection via sponging microRNA-33b.Bioengineered · 2022Article
- Long non-coding RNAs: Modulators of phenotypic transformation in vascular smooth muscle cells.Frontiers in cardiovascular medicine · 2022Review
- miR-3150b-3p Promotes Vascular Smooth Muscle Cell Injury by Targeting ARL5B.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/HemostasisArticle
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Authors and funding
5 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
It has been recognized that rebalancing the abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) helps relieve vascular injury. Presently, we aim to investigate whether long non-coding RNA (lncRNA) maternally expressed 8 (MEG8) plays a role in affecting the excessive proliferation and migration of VSMCs following hypoxia stimulation. A percutaneous transluminal angioplasty balloon dilatation catheter was adopted to establish vascular intimal injury, the levels of MEG8 and miR-195-5p in the carotid artery were tested by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Hypoxia was used to stimulate VSMCs, then the cell counting kit-8 (CCK-8) assay, Transnwell assay, and wound healing assay were conducted to evaluate the proliferation, and migration of VSMCs. The protein levels of RECK (reversion inducing cysteine rich protein with kazal motifs), MMP (matrix metalloproteinase) 3/9/13, COX2 (cytochrome c oxidase subunit II), macrophage inflammatory protein (MIP)-1beta, VCAM-1 (vascular cell adhesion molecule 1), ICAM-1 (intercellular adhesion molecule 1), and HIF-1α (hypoxia inducible factor 1 subunit alpha) were determined by western blot or cellular immunofluorescence. As the data showed, MEG8 was down-regulated in the carotid artery after balloon injury in rats and hypoxia-treated VSMCs, and miR-195-5p was overexpressed. Forced MEG8 overexpression or inhibiting miR-195-5p attenuated hypoxia-promoted cell proliferation and migration of VSMCs. In addition, miR-195-5p up-regulation reversed MEG8-mediated effects. Hypoxia hindered the RECK expression while boosted MMP3/9/13 levels, and the effect was markedly reversed with MEG8 up-regulation or miR-195-5p down-regulation. Mechanistically, MEG8 functioned as a competitive endogenous (ceRNA) by sponging miR-195-5p which targeted RECK. Moreover, the HIF-1α inhibitor PX478 prevented hypoxia-induced proliferation, and migration of VSMCs, upregulated MEG8, and restrained miR-195-5p expression. Overall, lncRNA MEG8 participated in hypoxia-induced excessive proliferation, inflammation and migration of VSMCs through the miR-195-5p/RECK axis.
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