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LncRNA FOXD3-AS1 modulates ER stress and epithelial barrier dysfunction in allergic rhinitis by destabilizing CHOP
Hao Zhang1, Yaqiong Zhu1, Chunping Yang1
1Department of Otolaryngology Head and Neck surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.
Background:
Allergic rhinitis (AR) is an allergic disease of nasal mucosa. LncRNAs are key modulators affecting AR development. Nevertheless, the impact of LncRNA FOXD3-AS1 in AR is not clear.
Methods:
Human nasal epithelial cells (hNECs) were exposed to ovalbumin (OVA) to establish AR cell model, AR mice model was also constructed by OVA treatment. RIP assay was conducted to verify the association between FOXD3-AS1 and RBM15B. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot analyses were performed to detect the expression of ER stress markers: Autophagy Related Gene 4 (ATG4), phosphorylated Protein kinase R-like endoplasmic reticulum kinase (p-PERK), and phosphorylated eukaryotic initiation factor 2α (p-eIF2α) in hNECs after overexpression of FOXD3-AS1. HNECs were treated with ER stress inhibitor 4-phenylbutyric acid (4-PBA).
Results:
The expressions of LncRNA FOXD3-AS1 were downregulated in AR model. Moreover, overexpression FOXD3-AS1 reversed the effect of AR on ER stress markers. RBM15B was found to be bound with FOXD3-AS1. After 4-PBA treatment, the protein expression of ATG4, CHOP, p-PERK, and p-eIF2α was significantly reduced in cultured AR cell model.
Conclusion:
This study illustrated that FOXD3-AS1 acted as an inhibitor in AR induced ER stress and epithelial barrier dysfunction by destabilizing CHOP mRNA via RBM15B.
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