TGF-β1通过microRNA-182诱导慢性鼻炎伴鼻息肉的上皮细胞向间质转化

IF 2.3 4区 医学 Q3 ALLERGY
Wenxiu Jiang, Chun Zhou, Chengxin Ma, Yujie Cao, Guohong Hu, Huabin Li
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引用次数: 0

摘要

背景:鼻上皮细胞的上皮-间质转化(EMT)参与了慢性鼻炎伴鼻息肉(CRSwNP)的组织重塑。我们的研究调查了microRNA-182(miR-182)调控嗜酸性(Eos)和非嗜酸性(non-Eos)CRSwNP中EMT的分子机制:研究 miR-182 调节人鼻腔上皮细胞(hNEPCs)EMT 的机制:方法:采用Western印迹法和逆转录定量PCR(RT-qPCR)法测定EMT标记物(E-cadherin、N-cadherin和vimentin)、转化生长因子(TGF)-β1和miR-182的表达。荧光原位杂交(FISH)用于检测 miR-182 的定位。此外,在使用 TGF-β1、TGF-β1 与 miR-182 抑制剂、miR-182 模拟物或单独使用 miR-182 抑制剂处理 hNEPCs 时,检测了 EMT 标记物的表达和细胞形态的变化:结果:与对照鼻组织相比,Eos CRSwNP和非Eos CRSwNP中E-cadherin的表达水平均下调,而N-cadherin、vimentin、TGF-β1和miR-182的表达水平均显著上调。此外,与非 Eos CRSwNP 相比,在 Eos-CRSwNP 中观察到这些 EMT 标记发生了更明显的变化。在诱导 hNEPCs 模型中,TGF-β1 上调了 miR-182 的表达并促进了 hNEPCs 的 EMT,这表现在细胞形态和 EMT 标记表达的变化上。此外,这些上调被miR-182抑制剂逆转:本研究表明,miR-182 对 TGF-β1 诱导的 EMT 可促进 Eos CRSwNP 和非 Eos CRSwNP 的鼻息肉发生,从而为未来开发治疗 CRSwNP 的新型疗法提供了潜在靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
TGF-β1 induces epithelial-to-mesenchymal transition in chronic rhinosinusitis with nasal polyps through microRNA-182.

Background: Epithelial-to-mesenchymal transition (EMT) in nasal epithelial cells is involved in tissue remodeling of chronic rhinosinusitis with nasal polyps (CRSwNP). Our study investigated the molecular mechanisms that microRNA-182 (miR-182) regulated EMT in eosinophilic (Eos) and non-eosinophilic (non-Eos) CRSwNP.

Objective: To investigate the mechanism by which miR-182 regulates EMT in human nasal epithelial cells (hNEPCs).

Methods: The expression of EMT markers (E-cadherin, N-cadherin and vimentin), transforming growth factor (TGF)-β1, and miR-182 were determined by western blotting and reverse transcription-quantitative PCR (RT-qPCR). Fluorescence in situ hybridization (FISH) was used to detect the miR-182 localization. Additionally, EMT markers expression and cell morphology changes were checked upon treatment with TGF-β1, or TGF-β1 with miR-182 inhibitor, or miR-182 mimics, or miR-182 inhibitor alone in hNEPCs.

Results: In both Eos CRSwNP and non-Eos CRSwNP, the expression levels of E-cadherin were downregulated while the expression levels of N-cadherin, vimentin, TGF-β1 and miR-182 were significantly upregulated compared with control nasal tissues. Additionally, more significant changes in these EMT markers were observed in the Eos-CRSwNP when compared with the non-Eos CRSwNP. Invitro hNEPCs model, TGF-β1 upregulated miR-182 expression and promoted EMT in hNEPCs, indicated by changes in cell morphology and EMT markers expression. Furthermore, these upregulations were reversed by miR-182 inhibitor.

Conclusions: This study showed that miR-182-induced EMT in response to TGF-β1 might promote nasal polypogenesis in both Eos CRSwNP and non-Eos CRSwNP, thus providing potential targets for the future development of novel therapeutic approaches for the management of CRSwNP.

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来源期刊
CiteScore
12.80
自引率
0.00%
发文量
74
审稿时长
>12 weeks
期刊介绍: The Asian Pacific Journal of Allergy and Immunology (APJAI) is an online open access journal with the recent impact factor (2018) 1.747 APJAI published 4 times per annum (March, June, September, December). Four issues constitute one volume. APJAI publishes original research articles of basic science, clinical science and reviews on various aspects of allergy and immunology. This journal is an official journal of and published by the Allergy, Asthma and Immunology Association, Thailand. The scopes include mechanism, pathogenesis, host-pathogen interaction, host-environment interaction, allergic diseases, immune-mediated diseases, epidemiology, diagnosis, treatment and prevention, immunotherapy, and vaccine. All papers are published in English and are refereed to international standards.
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