在未分化的人鼻上皮细胞培养中，MiR-214在慢性鼻窦炎粘膜中的表达升高并调节脂多糖介导的反应

IF 2.5 3区医学 Q1 OTORHINOLARYNGOLOGY

American Journal of Rhinology & Allergy Pub Date : 2023-07-01 DOI:10.1177/19458924231152683

Zhou Wang, Dong Lin, Yuxiang Zhao, Hui Liu, Ting Yang, An Li

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MUC5AC protein level was detected using western blot. Similarly, we determined the relationship between miR-214 and Sirtuin 1 (SIRT1) using the Dual luciferase activity assay. Results miR-214 was increased in CRSwNP and CRSsNP tissues. LPS triggered the expression of miR-214, while miR-214 inhibition diminished the level of miR-214. MiR-214 inhibition prevented LPS-mediated the production of inflammatory cytokines. LPS treatment augmented MUC5AC mRNA, protein levels, and secretion, whereas miR-214 loss inhibited MUC5AC production in the presence of LPS. SIRT1 is a direct target of miR-214. Impairing SIRT1 by siRNA (siSIRT1) or EX527 (a selective SIRT1 inhibitor) reversed the effects of miR-214 inhibitor on inflammation and MUC5AC expression. Furthermore, miR-214 depression inhibited the STAT3/GDF15 pathway via targeting SIRT1. Upregulation of STAT3 or GDF15 partly abolished the anti-inflammatory roles of miR-214 inhibitor. 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MicroRNAs (miRs) are reported to regulate several diverse physiological and pathological processes. Objective This study aimed to evaluate the impact of miR-214 on lipopolysaccharide (LPS)-mediated inflammation, and mucin 5AC (MUC5AC) expression in human nasal epithelial cells. Methods The expression of miR-214 was detected in CRS with polyps (CRSwNP) and CRS without polyps (CRSsNP) tissues. Cells were treated with LPS and a miR-214 inhibitor. The level of miR-214 was detected by quantitative real-time reverse transcriptase-PCR (qRT-PCR). The inflammatory cytokines (IL-6, IL-8, TNF, and IL-1β) and MUC5AC production were determined by qRT-PCR and ELISA. MUC5AC protein level was detected using western blot. Similarly, we determined the relationship between miR-214 and Sirtuin 1 (SIRT1) using the Dual luciferase activity assay. Results miR-214 was increased in CRSwNP and CRSsNP tissues. LPS triggered the expression of miR-214, while miR-214 inhibition diminished the level of miR-214. 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引用次数: 1

摘要

背景:慢性鼻窦炎(CRS)是一种上呼吸道炎症性疾病。据报道，MicroRNAs (miRs)调节多种不同的生理和病理过程。目的:本研究旨在评估miR-214对人鼻上皮细胞中脂多糖(LPS)介导的炎症和粘蛋白5AC (MUC5AC)表达的影响。方法:检测miR-214在有息肉的CRS (CRSwNP)和无息肉的CRS (CRSsNP)组织中的表达。细胞用LPS和miR-214抑制剂处理。采用实时定量逆转录pcr (qRT-PCR)检测miR-214水平。采用qRT-PCR和ELISA检测炎症因子(IL-6、IL-8、TNF和IL-1β)和MUC5AC的产生。western blot检测MUC5AC蛋白水平。同样，我们使用双荧光素酶活性测定法确定了miR-214和Sirtuin 1 (SIRT1)之间的关系。结果:miR-214在CRSwNP和CRSsNP组织中表达升高。LPS触发miR-214的表达，而miR-214的抑制降低了miR-214的水平。MiR-214抑制抑制lps介导的炎症细胞因子的产生。LPS处理增加了MUC5AC mRNA、蛋白水平和分泌，而miR-214缺失抑制了LPS存在下MUC5AC的产生。SIRT1是miR-214的直接靶点。通过siRNA (siSIRT1)或EX527(一种选择性SIRT1抑制剂)损伤SIRT1可以逆转miR-214抑制剂对炎症和MUC5AC表达的影响。此外，miR-214抑制通过靶向SIRT1抑制STAT3/GDF15通路。STAT3或GDF15的上调部分消除了miR-214抑制剂的抗炎作用。结论:综上所述，miR-214通过靶向SIRT1调控lps介导的炎症和MUC5AC表达，STAT3/GDF15可能参与了miR-214抑制剂对炎症和MUC5AC表达的调控。

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MiR-214 Expression Is Elevated in Chronic Rhinosinusitis Mucosa and Regulates Lipopolysaccharide-Mediated Responses in Undifferentiated Human Nasal Epithelial Cell Culture.

Background Chronic rhinosinusitis (CRS) is an inflammatory disorder of the upper airways. MicroRNAs (miRs) are reported to regulate several diverse physiological and pathological processes. Objective This study aimed to evaluate the impact of miR-214 on lipopolysaccharide (LPS)-mediated inflammation, and mucin 5AC (MUC5AC) expression in human nasal epithelial cells. Methods The expression of miR-214 was detected in CRS with polyps (CRSwNP) and CRS without polyps (CRSsNP) tissues. Cells were treated with LPS and a miR-214 inhibitor. The level of miR-214 was detected by quantitative real-time reverse transcriptase-PCR (qRT-PCR). The inflammatory cytokines (IL-6, IL-8, TNF, and IL-1β) and MUC5AC production were determined by qRT-PCR and ELISA. MUC5AC protein level was detected using western blot. Similarly, we determined the relationship between miR-214 and Sirtuin 1 (SIRT1) using the Dual luciferase activity assay. Results miR-214 was increased in CRSwNP and CRSsNP tissues. LPS triggered the expression of miR-214, while miR-214 inhibition diminished the level of miR-214. MiR-214 inhibition prevented LPS-mediated the production of inflammatory cytokines. LPS treatment augmented MUC5AC mRNA, protein levels, and secretion, whereas miR-214 loss inhibited MUC5AC production in the presence of LPS. SIRT1 is a direct target of miR-214. Impairing SIRT1 by siRNA (siSIRT1) or EX527 (a selective SIRT1 inhibitor) reversed the effects of miR-214 inhibitor on inflammation and MUC5AC expression. Furthermore, miR-214 depression inhibited the STAT3/GDF15 pathway via targeting SIRT1. Upregulation of STAT3 or GDF15 partly abolished the anti-inflammatory roles of miR-214 inhibitor. Conclusion Taken together, miR-214 regulates LPS-mediated inflammation and MUC5AC expression via targeting SIRT1, and STAT3/GDF15 may involve in the regulation of miR-214 inhibitor on inflammation and MUC5AC expression.

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来源期刊

American Journal of Rhinology & Allergy 医学-耳鼻喉科学

CiteScore

5.60

自引率

11.50%

发文量

审稿时长

4-8 weeks

期刊介绍： The American Journal of Rhinology & Allergy is a peer-reviewed, scientific publication committed to expanding knowledge and publishing the best clinical and basic research within the fields of Rhinology & Allergy. Its focus is to publish information which contributes to improved quality of care for patients with nasal and sinus disorders. Its primary readership consists of otolaryngologists, allergists, and plastic surgeons. Published material includes peer-reviewed original research, clinical trials, and review articles.