The Expression and Regulation of Na+-K+-ATPase in Nasal Epithelial Cells of Chronic Rhinosinusitis with Nasal Polyps

The Expression and Regulation of Na+-K+-ATPase in Nasal Epithelial Cells of Chronic Rhinosinusitis with Nasal Polyps
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慢性鼻窦炎鼻息肉鼻上皮细胞Na-K-ATP酶的表达及调控

DOI:
10.1159/000517101
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发表时间:
2021-09
期刊:
ORL
影响因子:
--
通讯作者:
Weitian Zhang
Weitian Zhang
中科院分区:
其他
文献类型:
--
作者:
Guangyi Ba;Ru Tang;Song Mao;Zhipeng Li;Haibo Ye;Hai Lin;Weitian Zhang

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目的:Na+-K+-ATP酶(Na+-K+-ATPase,NKA)在维持细胞通透性、储存势能、防止细胞水肿等方面起重要作用.然而,NKA表达如何在慢性鼻窦炎鼻息肉(CRSwNP)中改变和调节仍然不确定。因此,本研究旨在探讨NKA在CRSwNP中的表达和调控。研究方法:免疫组化法检测鼻黏膜NKA蛋白表达,Western blotting法检测鼻黏膜NKA蛋白表达,实时荧光定量PCR法检测鼻黏膜NKA和水通道蛋白5(AQP 5)mRNA表达。通过免疫荧光染色评价NKA与炎性细胞的共定位。此外,培养人鼻上皮细胞(HNECs),并使用各种刺激物刺激,以评估NKA的调节。结果如下:我们发现与对照组相比,CRSwNP患者鼻组织中NKA阳性细胞、NKA蛋白水平和NKA和AQP 5的mRNA水平显著降低,尤其是在嗜酸性CRSwNP中。此外,葡萄球菌肠毒素B(SE B)、脂多糖(LPS)、炎症细胞因子(IFN)-γ、IL-4、IL-13和IL-1β可下调HNECs中NKA mRNA的表达。结论:CRSwNP中NKA和AQP 5表达减少。SEB、LPS、IFN-γ、IL-4、IL-13和IL-1β均能抑制HNECs的NKA。NKA损伤可能通过诱导AQP 5表达下调和水肿参与CRSwNP的发生发展。
Objective: Na+-K+-ATPase (NKA) is essential in maintaining cell permeability, reserving potential energy, and preventing cellular edema. Nevertheless, how NKA expression is altered and regulated in chronic rhinosinusitis with nasal polyps (CRSwNPs) remain uncertain. Therefore, the present study aimed to explore the expression and regulation of NKA in CRSwNP. Methods: NKA immunolabeling was assessed by the immunohistochemistry method, NKA protein levels were detected with the Western blotting method, and mRNA levels of NKA and aquaporin-5 (AQP5) were assayed by real-time PCR in nasal tissues from CRSwNP and control subjects. The co-localization of NKA with inflammatory cells was evaluated by immunofluorescence staining. In addition, human nasal epithelial cells (HNECs) were cultured and stimulated using various stimulators to evaluate the regulation of NKA. Results: We found significantly decreased NKA positive cells, NKA protein levels, and mRNA levels of NKA and AQP5 in nasal tissues from CRSwNP patients compared to control subjects, especially in eosinophilic CRSwNP. Furthermore, NKA mRNA levels in HNECs were downregulated by staphylococcal enterotoxin B (SEB), lipopolysaccharides (LPSs), inflammatory cytokine (IFN)-γ, IL-4, IL-13, and IL-1β. Conclusion: NKA and AQP5 expressions were decreased in CRSwNP. NKA in HNECs could be suppressed by SEB, LPS, IFN-γ, IL-4, IL-13, and IL-1β. Impairment of NKA may contribute to the genesis and development of CRSwNP via inducing AQP5 downregulation and edema.
DOI: --
发表时间: 2007
影响因子: 2.9
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发表时间: 2017
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