ArticleMedical science monitor : international medical journal of experimental and clinical research2018
Long Noncoding RNA XR007793 Regulates Proliferation and Migration of Vascular Smooth Muscle Cell via Suppressing miR-23b.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Role of ncRNAs in Neurological Disorders and Cardiovascular Diseases.Experientia supplementum (2012) · 2026Review
- Metabolomics analysis of acute lung injury induced by aortic dissection in mice.Annals of medicine and surgery (2012) · 2025Article
- Targeting PDGF/PDGFR Signaling Pathway by microRNA, lncRNA, and circRNA for Therapy of Vascular Diseases: A Narrow Review.Biomolecules · 2024Review
- ncRNAs and polyphenols: new therapeutic strategies for hypertension.RNA biology · 2022Article
- Long non-coding RNAAnnals of translational medicine · 2021Article
- Targeting the epigenome in in-stent restenosis: from mechanisms to therapy.Molecular therapy. Nucleic acids · 2021Review
- MiR-128-3p inhibits vascular smooth muscle cell proliferation and migration by repressing FOXO4/MMP9 signaling pathway.Molecular medicine (Cambridge, Mass.) · 2020Article
- Long noncoding RNAs as novel players in the pathogenesis of hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2020Review
- Current perspective on the regulation of FOXO4 and its role in disease progression.Cellular and molecular life sciences : CMLS · 2020Review
- Transcription Factors Targeted by miRNAs Regulating Smooth Muscle Cell Growth and Intimal Thickening after Vascular Injury.International journal of molecular sciences · 2019Review
- Long noncoding RNA LINC00341 promotes the vascular smooth muscle cells proliferation and migration via miR-214/FOXO4 feedback loop.American journal of translational research · 2019Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Long noncoding RNAs (lncRNAs) were identified as potential regulatory factor in vascular disease. However, the role of XR007793 in the regulation of neointima formation after vascular injury remains largely unknown. MATERIAL AND METHODS LncRNA expression levels were detected using real-time polymerase chain reaction (RT-PCR). In vivo and in vitro assay were performed in Sprague-Dawley rats and VSMCs. Cell Counting Kit-8 (CCK-8) assay, Transwell assay, and scratch wound healing assay were performed to detect cell proliferation and migration. Western blotting was used to detect protein expression. RESULTS The results of qRT-PCR indicated that XR007793 expression was significantly increased in the injured carotid artery of Sprague-Dawley rats and platelet-derived growth factor-BB induced rat aortic smooth muscle cells. Knockdown of XR007793 repressed the proliferation and migration of VSMC in vitro. The expression level of miR-23b was reduced in mouse carotid injured tissues and cell line. Bioinformatics analysis and luciferase reporter assay revealed that XR007793 directly bonds to miR-23b. Pearson correlation analysis showed that XR007793a and miR-23b were negatively correlated in carotid samples. Furthermore, bioinformatics analysis and luciferase assay indicated that miR-23b targeted the Forkhead box O 4 (FOXO4) 3'-UTR to inhibit FOXO4 expression. After transfecting miR-23b inhibitor, the expression both of XR007793 and FOXO4 was increased. The effects on expression were reversed after transfected with miR-23b mimics. Rescue experiments results indicated that miR-23b inhibitor reduced the expression of VSMC marker and promoted proliferation and migration of VSMC. CONCLUSIONS This study shows that XR007793 aggravates the loss of function of VSMCs by negatively regulating miR-23b. It does so by targeting FOXO4, which could serve as a novel therapeutic target in post-angioplasty restenosis.
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