Background: This study aims to investigate the regulatory effect of microRNA-96-5p (miR-96-5p) in the pathophysiological process of allergic rhinitis (AR). Methods: Nasal mucosal tissue samples were collected from AR patients and healthy controls. An in vitro AR model was established by stimulating human nasal epithelial cells (HNECs) with interleukin (IL)-13. The expressions of target genes and proteins were measured by qPCR, Western blot, or ELISA. Dual-luciferase reporter assay and pull-down assay were performed to confirm the interaction between miR-96-5p and DEP domain-containing mammalian target of rapamycin-interacting protein (DEPTOR). Results: The level of miR-96-5p was increased while the expression of DEPTOR was decreased in AR patients. The expressions of proinflammatory cytokines were markedly increased and the mammalian target of rapamycin (mTOR)/NF-κB pathway was activated in HNECs following IL-13 stimulation. miR-96-5p downregulation alleviated the stimulated function by IL-13. DEPTOR was the target of miR-96-5p. Knockdown of DEPTOR reversed the function of miR-96-5p inhibitor on IL-13-stimulated HNECs. Conclusions: The current study showed that miR-96-5p and DEPTOR were aberrantly expressed in AR nasal mucosa. miR-96-5p knockdown inhibited the production of inflammatory cytokines and the activation of mTOR/NF-κB pathway via targeting DEPTOR. These findings suggested that miR-96-5p might be used as a diagnostic marker and therapeutic target for the treatment of AR.
Int Arch Allergy Immunol

中文翻译：

---

miR-96-5p 的下调通过 DEPTOR 抑制过敏性鼻炎中的 mTOR/NF-κb 信号通路

背景：本研究旨在探讨microRNA-96-5p（miR-96-5p）在变应性鼻炎（AR）病理生理过程中的调控作用。方法：从 AR 患者和健康对照中收集鼻黏膜组织样本。通过用白细胞介素 (IL)-13 刺激人鼻上皮细胞 (HNEC) 建立体外 AR 模型。通过qPCR、Western印迹或ELISA测量靶基因和蛋白质的表达。进行双荧光素酶报告基因测定和下拉测定以确认 miR-96-5p 与含有 DEP 结构域的哺乳动物雷帕霉素相互作用蛋白靶标 (DEPTOR) 之间的相互作用。结果：AR患者miR-96-5p水平升高而DEPTOR表达降低。IL-13刺激后，HNEC中促炎细胞因子的表达显着增加，哺乳动物雷帕霉素靶标（mTOR）/NF-κB通路被激活。miR-96-5p 下调减轻了 IL-13 刺激的功能。DEPTOR 是 miR-96-5p 的靶点。DEPTOR 的敲低逆转了 miR-96-5p 抑制剂对 IL-13 刺激的 HNEC 的功能。结论：目前的研究表明 miR-96-5p 和 DEPTOR 在 AR 鼻粘膜中异常表达。miR-96-5p 敲低通过靶向 DEPTOR 抑制炎性细胞因子的产生和 mTOR/NF-κB 通路的激活。这些发现表明 miR-96-5p 可能用作治疗 AR 的诊断标志物和治疗靶点。
Int Arch 过敏免疫