ArticleThe Kaohsiung journal of medical sciences2022
MicroRNA-214-3p facilitates M2 macrophage polarization by targeting GSK3B.
Article in The Kaohsiung journal of medical sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Application of Extracellular Vesicles in Allergic Rhinitis: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- Interleukin-Mediated Macrophage Polarization in Allergic Rhinitis Inflammation: A Systematic Review.Journal of inflammation research · 2026Review
- IL-Mediated Macrophage Polarization Axis: From Inflammatory Positive Feedback Loop to Precision Biomarkers and Therapeutic Targets for Allergic Rhinitis-A Narrative Review.Journal of asthma and allergy · 2026Review
- miR-214-3p inhibits LPS-induced macrophage inflammation and attenuates the progression of dry eye syndrome by regulating ferroptosis in cells.Genes & genomics · 2025Article
- Role of microRNAs in Immune Regulation with Translational and Clinical Applications.International journal of molecular sciences · 2024Review
- Large-scale computational modelling of the M1 and M2 synovial macrophages in rheumatoid arthritis.NPJ systems biology and applications · 2024Article
- Review
- Spinal cord injury dysregulates fibro-adipogenic progenitors miRNAs signaling to promote neurogenic heterotopic ossifications.Communications biology · 2023Article
- The Extracellular Vesicle-Macrophage Regulatory Axis: A Novel Pathogenesis for Endometriosis.Biomolecules · 2023Review
- MicroRNA-214-3p facilitates M2 macrophage polarization by targeting GSK3B.The Kaohsiung journal of medical sciences · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Allergic rhinitis (AR) is a chronic inflammatory disease of the nasal mucosa. M2 macrophage polarization can reduce inflammation and repair tissue injury during AR development. Studies have substantiated the involvement of miRNAs in AR pathogenesis. Herein, the molecular mechanism of miR-214-3p in AR development was explored. To mimic the AR environment, ovalbumin (OVA) was used to treat macrophages. MiR-214-3p and glycogen synthase kinase 3 beta (GSK3B) expression in nasal mucus tissues and macrophages was assessed by RT-qPCR. The M2 phenotypic signature of CD206 in macrophages was assessed by flow cytometry. The protein expression of GSK3B and M2 macrophage markers (ARG-1 and IL-10) was evaluated by western blotting. The correlation between miR-214-3p and GSK3B was validated by a luciferase reporter assay. We found that miR-214-3p was overexpressed in macrophages and nasal mucus tissues from AR patients. MiR-214-3p facilitated M2 polarization of macrophages upon OVA stimulation. Mechanistically, miR-214-3p targeted the GSK3B 3' untranslated region in macrophages. In addition, GSK3B was downregulated in macrophages and nasal mucus tissues from AR patients. In rescue assays, GSK3B downregulation reversed the inhibitory effects of miR-214-3p silencing on M2 polarization of macrophages treated with OVA. Overall, miR-214-3p facilitates M2 macrophage polarization by targeting GSK3B.
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