The circular RNA circTXNRD1 promoted ambient particulate matter-induced inflammation in human bronchial epithelial cells by regulating miR-892a/COX-2 axis.

The circular RNA circTXNRD1 promoted ambient particulate matter-induced inflammation in human bronchial epithelial cells by regulating miR-892a/COX-2 axis.
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环状RNA circTXNRD1通过调节miR-892a/COX-2轴促进环境颗粒物诱导的人支气管上皮细胞炎症。

DOI:
10.1016/j.chemosphere.2021.131614
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发表时间:
2021-07
期刊:
影响因子:
8.8
通讯作者:
Yuanlin Song
Yuanlin Song
中科院分区:
环境科学与生态学2区
文献类型:
--
作者:
Jian Wang;Mengchan Zhu;Juan Song;Yingying Zeng;Shijin Xia;Cuicui Chen;Meiling Jin;Yuanlin Song

文献摘要

相似文献

颗粒物(PM)诱导的气道炎症有助于慢性气道疾病的发展和加重。环状RNA(circular RNA,circRNA)是一类新的非编码RNA,参与多种呼吸系统疾病的基因调控,但circRNA在PM诱导的气道炎症中的调控作用尚未完全阐明。在本研究中,我们利用人circRNA微阵列来揭示PM诱导的人支气管上皮细胞(HBECs)中差异表达的circRNA。共鉴定了176种上调和15种下调的circRNA。其中,一个新的circRNA称为circTXNRD 1的上调PM暴露在剂量和时间依赖性的方式。敲除circTXNRD 1显著减弱PM诱导的促炎细胞因子白细胞介素6(IL-6)的表达。CircRNA pull-down、双荧光素酶报告基因检测和荧光原位杂交结果显示,circTXNRD 1可作为内源性海绵降低miR-892 a在HBECs中的表达。下调miR-892 a可增加PM诱导的HBEC中环氧合酶-2(考克斯-2)的表达,并最终促进IL-6的分泌。综上所述,我们的研究结果揭示了circTXNRD 1通过调节miR-892 a/考克斯-2轴在PM诱导的HBEC炎症中作为一种新的炎症介质。这些结果提供了新的见解PM诱导的炎症在慢性气道疾病的生物学机制。
Particulate matter (PM)-induced airway inflammation contributes to the development and exacerbation of chronic airway diseases. Circular RNA (circRNA) is a new class of non-coding RNA that participates in gene regulation in various respiratory diseases, but the regulatory role of circRNA in PM-induced airway inflammation has not been fully elucidated. In this study, we performed the human circRNA microarray to reveal differentially expressed circRNAs in PM-induced human bronchial epithelial cells (HBECs). A total of 176 upregulated and 15 downregulated circRNAs were identified. Of these, a new circRNA termed circTXNRD1 was upregulated by PM exposure in a dose- and time-dependent manner. Knockdown of circTXNRD1 significantly attenuated PM-induced expression of proinflammatory cytokine interleukin 6 (IL-6). CircRNA pull-down, dual-luciferase reporter assay and fluorescence in situ hybridization showed that circTXNRD1 acted as an endogenous sponge to decrease miR-892a levels in HBECs. Downregulation of miR-892a could increase cyclooxygenase-2 (COX-2) expression and eventually promote IL-6 secretion in PM-induced HBECs. Taken together, our findings reveal circTXNRD1 as a novel inflammatory mediator in PM-induced inflammation in HBECs via regulating miR-892a/COX-2 axis. These results provide new insight into the biological mechanism underlying PM-induced inflammation in chronic airway diseases.