ArticleImmunity, inflammation and disease2023
RORα overexpression reduced interleukin-33 expression and prevented mast cell degranulation and inflammation by inducing autophagy in allergic rhinitis.
Article in Immunity, inflammation and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- RORα: a critical nexus in the crosstalk between cholesterol metabolism and macrophage polarization.Frontiers in immunology · 2026Review
- Retinoic acid-related orphan nuclear receptor alpha inhibits adipogenic differentiation of bone marrow mesenchymal stem cells via activating WNT/β-catenin signaling pathway.European journal of medical research · 2025Article
- NLRP3 Inflammasome Deficiency Alleviates Inflammation and Oxidative Stress by Promoting PINK1/Parkin-Mediated Mitophagy in Allergic Rhinitis Mice and Nasal Epithelial Cells.Journal of asthma and allergy · 2024Article
- Tyrosine kinases: multifaceted receptors at the intersection of several neurodegenerative disease-associated processes.Frontiers in dementia · 2024Review
- RORα overexpression reduced interleukin-33 expression and prevented mast cell degranulation and inflammation by inducing autophagy in allergic rhinitis.Immunity, inflammation and disease · 2023Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRetinoid acid receptor related orphan receptor α (RORα) is a nuclear receptor that along with other bioactive factors regulates cell proliferation, differentiation, and immunomodulation in vivo.
aimsThe objective of this study was to explore the function and mechanism of RORα in allergic rhinitis (AR). MATERIALS AND
methodsDerp1 was used to construct an AR cell model in HNEpC cells, and RORα was overexpressed or silenced in the AR HNEpC cells. Next, LAD2 cells were co-cultured with the Derp1-treated HNEpC cells. Additionally, an AR mouse model was established using by OVA, and a RORα Adenovirus was delivered by nebulizing. Pathological tissue structures were evaluated by hematoxylin-eosin staining, and the levels of RORα, interleukin-33 (IL-33), and other proteins were analyzed immunohistochemistry, western blotting, and immunofluorescence staining. IL-33, IL-4, IL-5, and IL-13 levels were detected using enzyme-linked immunosorbent assay kits and cell migration was assessed by Transwell assays.
resultsOur data showed that RORα was downregulated in the nasal mucosa tissues of AR patients. Derp1 treatment could cause a downregulation of RORα, upregulation of IL-33, the induction of NLRP3 inflammasomes, and cell migration in HNEpC cells. Furthermore, RORα overexpression dramatically attenuated IL-33 levels, NLRP3 inflammasome activity, and the migration of AR HNEpC cells induced with Derp1. Moreover, RORα in AR HNEpC cells could prevent mast cell (MC) degranulation and inflammation by accelerating autophagy, RORα overexpression inhibited MC degranulation and NLRP3-induced inflammation in the AR model mice. RORα overexpression reduced IL-33 expression in nasal epithelial cells, and also suppressed MC degranulation and inflammation by promoting autophagy.
conclusionRORα inhibits NLRP3 inflammasome in HNEpC, and attenuated mast cells degranulation and inflammation through autophagy in AR.
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