ArticleToxicological sciences : an official journal of the Society of Toxicology2020
Acute 4,4'-Methylene Diphenyl Diisocyanate Exposure-Mediated Downregulation of miR-206-3p and miR-381-3p Activates Inducible Nitric Oxide Synthase Transcription by Targeting Calcineurin/NFAT Signaling in Macrophages.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Circular RNA hsa_circ_0099188 regulates inducible nitric oxide synthase and chemokine transcription in macrophages by targeting the hsa-miR-381-3p/PPP3CA and hsa-miR-381-3p/KLF4 pathways in response to 4,4'-methylene diphenyl diisocyanate-glutathione conjugate exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- New mechanisms in diisocyanate-mediated allergy/toxicity: are microRNAs in play?Current opinion in allergy and clinical immunology · 2025Review
- Mast cell - tumor cell interaction related gene and microRNA expression profiles in oral squamous cell carcinoma.Frontiers in oncology · 2025Article
- Circular RNACells · 2024Article
- MicroRNA-mediated Krüppel-like factor 4 upregulation induces alternatively activated macrophage-associated marker and chemokine transcription in 4,4'-methylene diphenyl diisocyanate exposed macrophages.Xenobiotica; the fate of foreign compounds in biological systems · 2024Article
- Evaluation of penalized and machine learning methods for asthma disease prediction in the Korean Genome and Epidemiology Study (KoGES).BMC bioinformatics · 2024Article
- Article
- 4,4'-Methylene diphenyl diisocyanate exposure induces expression of alternatively activated macrophage-associated markers and chemokines partially through Krüppel-like factor 4 mediated signaling in macrophages.Xenobiotica; the fate of foreign compounds in biological systems · 2023Article
- Calcineurin Is a Universal Regulator of Vessel Function-Focus on Vascular Smooth Muscle Cells.Cells · 2023Review
- Skeletal myotube-derived extracellular vesicles enhance itaconate production and attenuate inflammatory responses of macrophages.Frontiers in immunology · 2023Article
- MicroRNA-194 inhibits isoproterenol-induced chronic cardiac hypertrophy via targeting CnA/NFATc2 signaling in H9c2 cells.Annals of translational medicine · 2022Article
- Calcineurin in development and disease.Genes & diseases · 2022Review
- The Specific microRNA Profile and Functional Networks for Children with Allergic Asthma.Journal of asthma and allergy · 2022Article
- MicroRNA-mediated calcineurin signaling activation induces CCL2, CCL3, CCL5, IL8, and chemotactic activities in 4,4'-methylene diphenyl diisocyanate exposed macrophages.Xenobiotica; the fate of foreign compounds in biological systems · 2021Article
- Epithelial miR-206 targets CD39/extracellular ATP to upregulate airway IL-25 and TSLP in type 2-high asthma.JCI insight · 2021Article
- Epigenetic Markers Are Associated With Differences in Isocyanate Biomarker Levels in Exposed Spray-Painters.Frontiers in genetics · 2021Article
- Arginine Metabolism and Its Potential in Treatment of Colorectal Cancer.Frontiers in cell and developmental biology · 2021Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Exposure to 4,4'-methylene diphenyl diisocyanate (MDI) in the occupational setting may lead to development of occupational asthma (OA), and the underlying molecular mechanisms of MDI-induced disease pathogenesis remain an active area of research. Using a nose-only mouse inhalation model, we find that circulating microRNA (miR)-206-3p and miR-381-3p are downregulated after MDI exposure; however, cellular miR-206-3p and miR-381-3p responses after MDI aerosol exposure and their pathophysiological roles in MDI-OA are unknown. We hypothesize that miR-206-3p and miR-381-3p-regulated mechanisms cause increased expression of the inducible nitric oxide synthase (iNOS) after MDI aerosol exposure. We examined cellular miR-206-3p and miR-381-3p, calcineurins, nuclear factors of activated T cells (NFATs), and iNOS levels from both nose-only exposed murine bronchoalveolar lavage cells (BALCs) and differentiated THP-1 macrophages treated with MDI-glutathione (GSH) conjugates. Both in vivo murine MDI aerosol exposure and in vitro MDI-GSH exposures in THP-1 macrophages result in downregulation of endogenous miR-206-3p and miR-381-3p and upregulation of PPP3CA and iNOS expression. Transfection of THP-1 macrophages with miR-inhibitor-206-3p and miR-inhibitor-381-3p resulted in the upregulation of PPP3CA and iNOS. Using RNA-induced silencing complex immunoprecipitation and translational reporter assays, we verified that PPP3CA, but not iNOS, is directly targeted by both miR-206-3p and miR-381-3p. Downregulation of miR-206-3p and miR-381-3p following by MDI exposure induces calcineurin/NFAT signaling-mediated iNOS transcription in macrophages and BALCs.
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