ArticleJCI insight2019
miR-511-3p protects against cockroach allergen-induced lung inflammation by antagonizing CCL2.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- PPAR-γ suppresses macrophage senescence and allergic airway inflammation through controlling lipid metabolic pathways.EBioMedicine · 2026Article
- Epithelial AhR Suppresses Allergen-Induced Oxidative Stress and Senescence via c-Myc Regulation.Antioxidants (Basel, Switzerland) · 2025Article
- Article
- Immunometabolic programming of macrophages in asthma pathogenesis and therapy.Frontiers in physiology · 2025Review
- Effective delivery of miR-511-3p with mannose-decorated exosomes with RNA nanoparticles confers protection against asthma.Journal of controlled release : official journal of the Controlled Release Society · 2024Article
- Regulation of Macrophage Polarization in Allergy by Noncoding RNAs.Non-coding RNA · 2023Review
- Dental pulp stem cells accelerate wound healing through CCL2-induced M2 macrophages polarization.iScience · 2023Article
- Advancing Treatment Strategies: A Comprehensive Review of Drug Delivery Innovations for Chronic Inflammatory Respiratory Diseases.Pharmaceutics · 2023Review
- Macrophages Orchestrate Airway Inflammation, Remodeling, and Resolution in Asthma.International journal of molecular sciences · 2023Review
- MicroRNAs in Macrophages: Regulators of Activation and Function.Journal of immunology (Baltimore, Md. : 1950) · 2023Review
- Nesfatin-1 Stimulates CCL2-dependent Monocyte Migration And M1 Macrophage Polarization: Implications For Rheumatoid Arthritis Therapy.International journal of biological sciences · 2023Article
- MicroRNA: role in macrophage polarization and the pathogenesis of the liver fibrosis.Frontiers in immunology · 2023Review
- Article
- Type II alveolar epithelial cell aryl hydrocarbon receptor protects against allergic airway inflammation through controlling cell autophagy.Frontiers in immunology · 2022Article
- Peptidylarginine deiminase 4 deficiency in bone marrow cells prevents plaque progression without decreasing atherogenic inflammation in apolipoprotein E-knockout mice.Frontiers in cardiovascular medicine · 2022Article
- Blockade of Mbd2 by siRNA-loaded liposomes protects mice against OVA-induced allergic airway inflammationFrontiers in immunology · 2022Article
- Type II alveolar epithelial cell-specific loss of RhoA exacerbates allergic airway inflammation through SLC26A4.JCI insight · 2021Article
- MiR-122-5p Mitigates Inflammation, Reactive Oxygen Species and SH-SY5Y Apoptosis by Targeting CPEB1 After Spinal Cord Injury Via the PI3K/AKT Signaling Pathway.Neurochemical research · 2021Article
- CaMKII oxidation regulates cockroach allergen-induced mitophagy in asthma.The Journal of allergy and clinical immunology · 2021Article
- Prescription ofJournal of healthcare engineering · 2021Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
miR-511-3p, encoded by CD206/Mrc1, was demonstrated to reduce allergic inflammation and promote alternative (M2) macrophage polarization. Here, we sought to elucidate the fundamental mechanism by which miR-511-3p attenuates allergic inflammation and promotes macrophage polarization. Compared with WT mice, the allergen-challenged Mrc1-/- mice showed increased airway hyperresponsiveness (AHR) and inflammation. However, this increased AHR and inflammation were significantly attenuated when these mice were pretransduced with adeno-associated virus-miR-511-3p (AAV-miR-511-3p). Gene expression profiling of macrophages identified Ccl2 as one of the major genes that was highly expressed in M2 macrophages but antagonized by miR-511-3p. The interaction between miR-511-3p and Ccl2 was confirmed by in silico analysis and mRNA-miR pulldown assay. Further evidence for the inhibition of Ccl2 by miR-511-3p was given by reduced levels of Ccl2 in supernatants of miR-511-3p-transduced macrophages and in bronchoalveolar lavage fluids of AAV-miR-511-3p-infected Mrc1-/- mice. Mechanistically, we demonstrated that Ccl2 promotes M1 macrophage polarization by activating RhoA signaling through Ccr2. The interaction between Ccr2 and RhoA was also supported by coimmunoprecipitation assay. Importantly, inhibition of RhoA signaling suppressed cockroach allergen-induced AHR and lung inflammation. These findings suggest a potentially novel mechanism by which miR-511-3p regulates allergic inflammation and macrophage polarization by targeting Ccl2 and its downstream Ccr2/RhoA axis.
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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.