ArticlePloS one2013
Reduction of microRNA-206 contributes to the development of bronchopulmonary dysplasia through up-regulation of fibronectin 1.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 45 citations in OpenAlex.
- Establishment and Evaluation of Cell Models for Bronchopulmonary Dysplasia: Challenges and Prospects.The clinical respiratory journal · 2025Review
- miRNA Signatures in Bronchopulmonary Dysplasia: Implications for Biomarkers, Pathogenesis, and Therapeutic Options.Frontiers in bioscience (Landmark edition) · 2024Review
- Mesenchymal stromal/stem cells and bronchopulmonary dysplasia.Frontiers in cell and developmental biology · 2023Review
- Review
- Silencing of MicroRNA-503 in Rat Mesenchymal Stem Cells Exerts Potent Antitumorigenic Effects in Lung Cancer Cells.OncoTargets and therapy · 2021Article
- Insight Into the Roles of Non-coding RNA in Bronchopulmonary Dysplasia.Frontiers in medicine · 2021Review
- MicroRNA Targets for Asthma Therapy.Advances in experimental medicine and biology · 2021Article
- LncRNA-MALAT1, as a biomarker of neonatal BPD, exacerbates the pathogenesis of BPD by targeting miR-206.American journal of translational research · 2021Article
- Inhibition of microRNA-29a alleviates hyperoxia-induced bronchopulmonary dysplasia in neonatal mice via upregulation of GAB1.Molecular medicine (Cambridge, Mass.) · 2019Article
- Thiol-Redox Regulation in Lung Development and Vascular Remodeling.Antioxidants & redox signaling · 2019Review
- Celecoxib Protects Hyperoxia-Induced Lung Injury via NF-κB and AQP1.Frontiers in pediatrics · 2019Article
- Hyperoxia causes miR-34a-mediated injury via angiopoietin-1 in neonatal lungs.Nature communications · 2017Article
- miR-206 inhibits FN1 expression and proliferation and promotes apoptosis of rat type II alveolar epithelial cells.Experimental and therapeutic medicine · 2017Article
- MicroRNA in late lung development and bronchopulmonary dysplasia: the need to demonstrate causality.Molecular and cellular pediatrics · 2016Review
- MicroRNA-206 functions as a tumor suppressor in colorectal cancer by targeting FMNL2.Journal of cancer research and clinical oncology · 2016Article
- Biomarkers for Bronchopulmonary Dysplasia in the Preterm Infant.Frontiers in pediatrics · 2016Review
- Attenuation of miR-17∼92 Cluster in Bronchopulmonary Dysplasia.Annals of the American Thoracic Society · 2015Article
- Host-virus interaction: the antiviral defense function of small interfering RNAs can be enhanced by host microRNA-7 in vitro.Scientific reports · 2015Article
- MicroRNA-206 regulates surfactant secretion by targeting VAMP-2.FEBS letters · 2015Article
- The Extracellular Matrix in Bronchopulmonary Dysplasia: Target and Source.Frontiers in medicine · 2015Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo characterize microRNA-206 (miR-206) in the development of bronchopulmonary dysplasia (BPD). DESIGN/
methodsWe assessed the expression of miR-206 in BPD mouse lung tissues and blood samples of BPD patients by quantitative real-time PCR. Then, the role of miR-206 in regulating cell biology were examined by XTT assay, flow cytometry, transwell invasion assay, wound healing assay and adhesion assay in vitro. Furthermore, luciferase reporter assay, real-time PCR, western blot and Immunofluorescence staining were performed to figure out the target gene of miR-206.
resultsA reduction in expression of miR-206 was observed in BPD mice compared with controls and in BPD patients compared with controls. miR-206 overexpression significantly induced cell apoptosis, reduced cell proliferation, migration and adhesion abilities, whereas the inhibition of miR-206 expression had the opposite effect. Fibronectin 1 (FN1) is a direct target of miR-206, and fn 1 can be transcriptionally and translationally regulated by miR-206. Down-regulation of miR-206 modulates biological functions of the cells, at least in part, by increasing the level of fn 1. Furthermore, fn 1 expression levels were increased in the BPD mice and BPD patients.
conclusionsThe expression of miR-206 and its target gene, fn 1, may contribute to the progression of BPD.
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