ArticleJournal of cellular and molecular medicine2020
A novel inhibitory role of microRNA-224 in particulate matter 2.5-induced asthmatic mice by inhibiting TLR2.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 44 citations in OpenAlex.
- Breast milk miRNAs and their potential role in the development of atopy in infants.Frontiers in molecular biosciences · 2026Review
- Elevated Serum Levels of miRNA-155 in Children with Atopic Dermatitis: A Potential Biomarker of Disease.International journal of molecular sciences · 2025Article
- PM2.5 Exposure Aggravates Inflammatory Response and Mucus Production in 16HBE Cells through Inducing Oxidative Stress and RAGE Expression.Cell biochemistry and biophysics · 2025Article
- Particulate matter-induced epigenetic modifications and lung complications.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- TheAnimals : an open access journal from MDPI · 2023Article
- SOX17 is a Critical Factor in Maintaining Endothelial Function in Pulmonary Hypertension by an Exosome-Mediated Autocrine Manner.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- The relationship between PM2.5 and the onset and exacerbation of childhood asthma: a short communication.Frontiers in pediatrics · 2023Article
- Anti-asthmatic miR-224-5p inhibits the FHL1/MAPK pathway to repress airway smooth muscle cell proliferation in a murine model of asthma-like airway inflammation.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2022Article
- Explore the Effect of Asthma Regulating HIF-1 Pathway on Sperm Quality Based on Rat Model.BioMed research international · 2022Article
- Article
- MicroRNAs: Potential mediators between particulate matter 2.5 and Th17/Treg immune disorder in primary membranous nephropathy.Frontiers in pharmacology · 2022Article
- Overexpression of miR-224-5p alleviates allergic rhinitis in mice via the TLR4/MyD88/NF-κB pathway.Experimental animals · 2021Article
- [Aryl hydrocarbon receptor modulates airway inflammation in mice with cockroach allergen-induced asthma by regulating Th17/Treg differentiation].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021Article
- HDAC1-mediated deacetylation of HIF1α prevents atherosclerosis progression by promoting miR-224-3p-mediated inhibition of FOSL2.Molecular therapy. Nucleic acids · 2021Article
- Airway hyperresponsiveness development and the toxicity of PM2.5.Environmental science and pollution research international · 2021Review
- Exosomes: A Key Piece in Asthmatic Inflammation.International journal of molecular sciences · 2021Review
- Role of Epigenetics in the Pathogenesis, Treatment, Prediction, and Cellular Transformation of Asthma.Mediators of inflammation · 2021Review
- Role of non-coding-RNAs in response to environmental stressors and consequences on human health.Redox biology · 2020Review
- A novel inhibitory role of microRNA-224 in particulate matter 2.5-induced asthmatic mice by inhibiting TLR2.Journal of cellular and molecular medicine · 2020Article
- Overexpression of the Aryl Hydrocarbon Receptor (Ahr) Mediates an Oxidative Stress Response following Injection of Fine Particulate Matter in the Temporal Cortex.Oxidative medicine and cellular longevity · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidemiological studies have shown that elevated concentrations of particulate matter 2.5 (PM2.5) correlate with increased incidence of asthma. Studies have highlighted the implication of microRNAs (miRNAs) in asthmatic response. Here, the objective of this study is to explore the effect of miR-224 on PM2.5-induced asthmatic mice. Ovalbumin (OVA) was utilized to establish asthmatic mouse models, which were then exposed to PM2.5, followed by miR-224 expression detection. Next, lesions and collagen deposition area in lung tissue, ratio Treg/Th17, the expression of TLR4 and MYD88, inflammation, eosinophils (EOS) and airway remodelling were evaluated in OVA mice after injection with miR-224 agomir. Following isolation of mouse primary bronchial epithelial cells, miR-224 mimic and TLR2/TLR4 inhibitor were introduced to assess inflammation and the expression of TGF-β, MMP9, TIMP-1, Foxp3, RORγt, TLR2, TLR4 and MYD88. After exposure to PM2.5, lesions and collagen deposition were promoted in lung tissues, inflammation and EOS were increased in bronchoalveolar lavage fluid (BALF), and airway remodelling was enhanced in OVA mice. miR-224 was down-regulated, whereas TLR2/TLR4/MYD88 was up-regulated in OVA mice after treatment with PM2.5, accompanied by Treg/Th17 immune imbalance. Of note, bioinformatic prediction and dual luciferase reporter gene assay confirmed that TLR2 was a target gene of miR-224. Overexpressed miR-224 reduced expression of TGF-β, MMP9, TIMP-1 and RORγt and inflammation but increased Foxp3 expression in bronchial epithelial cells through down-regulating TLR2. In summary, overexpressed miR-224 suppressed airway epithelial cell inflammation and airway remodelling in PM2.5-induced asthmatic mice through decreasing TLR2 expression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.