ArticleHeliyon2024
The role of ZEB1 in regulating tight junctions in antrochoanal polyp.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 1 citations in OpenAlex.
- Meta-analysis of the Relationship Between Neutrophil to Lymphocyte Ratio and Nasal Polyps.Indian journal of otolaryngology and head and neck surgery : official publication of the Association of Otolaryngologists of India · 2024Article
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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Antrochoanal polyp (ACP) is a benign nasal mass of unknown etiology. Tight junctions (TJs) are essential to the epithelial barrier that protects the body from external damage. However, the phenotype of tight junction in ACP is currently unclear. Methods: The samples were collected from 20 controls, 37 patients with ACP and 45 patients with chronic rhinosinusitis with nasal polyp (CRSwNP). Quantitative Real-Time PCR (qRT-PCR) and immunofluorescence staining (IF) were performed to analyze the expressions of TJs markers (ZO-1, claudin-3 and occludin) and ZEB1. hNEpCs were transfected with ZEB1 small interfering RNA (si-ZEB1) or ZEB1 over-expression plasmid (OE-ZEB1). qRT-PCR and Western blotting were used to determine the levels of TJs-related markers. Primary human nasal epithelial cells (hNECs) were stimulated with IL-17A and si-ZEB1, and the expression of epithelial barrier markers were measured by qRT-PCR and Western blotting. Results: Compared to the control group, ACP group showed a significant downregulation in both mRNA and protein levels of ZO-1, occludin, and claudin-3. Furthermore, disease severity correlates positively with the degree of disruption of tight junctions. In addition, higher expression levels of ZEB1, IL-17A, and IFN-γ were observed in the ACP group compared to controls. Overexpression of ZEB1 in hNEpCs led to impairments in the levels of ZO-1, occludin, and claudin-3, while silencing of ZEB1 expression was found to enhance the barrier function of epithelial cells. Finally, IL-17 stimulation of hNECs impaired the expression of TJs-associated molecules (ZO-1, occludin, and claudin-3), which was effectively reversed by the IL-17A + si-ZEB1 group. Conclusions: The tight junctions in ACP were extremely damaged and were correlated with the severity of the disease. ZEB1 was involved in the pathogenesis of ACP mediated by IL-17A through regulating tight junctions.
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