ArticleIranian journal of biotechnology2023
TNF-α Regulates the Glucocorticoid Receptor Alpha Expression in Human Nasal Epithelial Cells Via p65-NF-κb and p38-MAPK Signaling Pathways.
Article in Iranian journal of biotechnology, 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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5 citing papers in PubMed, 3 citations in OpenAlex.
- In Vitro Evaluation of the Inhibitory Effects of Linarin on Histamine-Induced Expression of Proinflammatory Cytokines, Mucin 5AC, and Aquaporin 5 in Human Nasal and Bronchial Epithelial Cells.The Kaohsiung journal of medical sciences · 2026Article
- The cellular triangle in bronchiectasis: the interplay network and regulatory mechanisms of neutrophils, macrophages, and epithelial cells.European journal of medical research · 2025Review
- Long-Term Cigarette Smoke Exposure Promotes Neutrophil Ferroptosis Resistance, Inducing Neutrophil Extracellular Trap Formation and Driving Glucocorticoid Resistance in Chronic Obstructive Pulmonary Disease.Research (Washington, D.C.) · 2025Article
- [Advances in glucocorticoid resistance in otorhinolaryngological diseases].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2024Review
- Ganglioside GD3 Regulates Inflammation and Epithelial-to-Mesenchymal Transition in Human Nasal Epithelial Cells.International journal of molecular sciences · 2024Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Tumor necrosis factor (TNF)-α induces changes in the glucocorticoid receptor (GR) isoforms' expression in human nasal epithelial cells (HNECs) in chronic rhinosinusitis (CRS). Objective: However, the underlying mechanism of TNF-α induced GR isoforms' expression in HNECs remains unclear. Here, we explored changes in inflammatory cytokines and glucocorticoid receptor alpha isoform (GRα) expression in HNECs. Materials and Methods: To explore the expression of TNF-α in nasal polyps and nasal mucosa of CRS, fluorescence immunohistochemical analysis was employed. To investigate changes in inflammatory cytokines and GRα expression in HNECs, RT-PCR and western blotting were performed following the cells' incubation with TNF-α. Cells were pretreated with the nuclear factor-κB gene binding (NF-κB) inhibitor QNZ, the p38 inhibitor SB203580, and dexamethasone for one hour, then a TNF-α. Western blotting, RT-PCR, and immunofluorescence had been utilized for the cells' analysis and the ANOVA for the data analysis. Results: The TNF-α fluorescence intensity was mainly distributed in nasal epithelial cells of nasal tissues. TNF-α prominently inhibited the expression of Conclusion: TNF-α induced changes in the GR isoforms' expression in HNECs, and it was mediated through p65-NF-κB and p38-MAPK signal transduction pathways, which could be considered a promising neutrophilic CRS treatment.
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