ArticleClinics (Sao Paulo, Brazil)2026
miR-628-3p exacerbates allergic rhinitis inflammation by targeting CELF2: A novel mechanistic insight.
Article in Clinics (Sao Paulo, Brazil), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAllergic Rhinitis (AR) represents a widespread chronic inflammatory condition, with especially prevalence observed in children and urban populations.
aimThis study primarily explored the expression of miR-628-3p in AR and its functional implications on the inflammatory response, and elucidated the underlying molecular mechanisms through which miR-628-3p regulates AR.
methodsRT-qPCR analysis quantified miR-628-3p expression in AR patient serum and cell models. The biological functionality of the cells was assessed using the CCK-8 assay and flow cytometry. Inflammatory cytokine levels were measured via ELISA. Bioinformatic prediction and dual-luciferase reporter assays were employed to validate miR-628-3p targets.
resultsmiR-628-3p expression was upregulated in the serum and cell samples of AR compared to healthy controls. miR-628-3p can target and bind to the downstream CELF2. Downregulation of miR-628-3p reduced apoptosis in AR cells and suppressed levels of inflammatory factors, while transfection of si-CELF2 reversed the protective ability of miR-628-3p inhibitor on AR cells.
conclusionsKnockdown of miR-628-3p may contribute to the pathogenesis of AR by mediating CELF2 to reduce the apoptosis and inflammatory response of AR cells, suggesting its potential protective role against AR-related cellular damage.
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