Arid2-IR downregulates miR-132-3p through methylation to promote LPS-induced ALI in pneumonia.

IF 2 4区医学 Q4 TOXICOLOGY

Inhalation Toxicology Pub Date : 2022-01-01 DOI:10.1080/08958378.2022.2102699

Yuanshui Liu, Chuanyu Bao, Gongping Deng, Yanhong Ouyang

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引用次数: 2

Abstract

Objective: Arid2-IR is a long non-coding RNA (lncRNA) that promotes renal injury, while its role in lipopolysaccharides (LPS)-induced acute lung injury (ALI) is unknown. Our preliminary sequencing analysis revealed an inverse correlation of Arid2-IR and miR-132-3p, which is known to suppress LPS-induced ALI. Therefore, Arid2-IR and miR-132-3p may interact with each other to participate in LPS-induced ALI in pneumonia. This study aimed to investigate the interaction between Arid2-IR and miR-132-3p in ALI induced by pneumonia.

Materials and methods: Plasma samples were obtained from patients with pneumonia (n = 98) and healthy controls (n = 98) to detect the expression of circulating Arid2-IR and miR-132-3p. The correlation between them was analyzed using Pearson's correlation coefficient. The crosstalk between them in human bronchial epithelial cells (HBEpC) was analyzed through overexpression assay. MSP was applied to determine the methylation of the miR-132-3p gene. Cell viability was evaluated by 2,5-diphenyl-2H-tetrazolium bromide assay.

Results: Arid2-IR was highly upregulated in pneumonia group, while the expression levels of miR-132-3p decreased in pneumonia group compared to that in the controls. Arid2-IR and miR-132-3p were inversely correlated across patient samples. Overexpression of Arid2-IR decreased the expression levels of miR-132-3p in HBEpCs and increased the methylation of miR-132-3p gene. Arid2-IR suppressed the role of miR-132-3p in increasing the viability of HBEpCs induced by LPS.

Discussion and conclusion: Arid2-IR is upregulated in pneumonia and may downregulate miR-132-3p by increasing its methylation to decrease cell viability, thereby promoting LPS-induced ALI in pneumonia.

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Arid2-IR通过甲基化下调miR-132-3p，促进lps诱导的肺炎ALI。

目的:Arid2-IR是一种促进肾损伤的长链非编码RNA (lncRNA)，但其在脂多糖(LPS)诱导的急性肺损伤(ALI)中的作用尚不清楚。我们的初步测序分析显示Arid2-IR和miR-132-3p呈负相关，已知miR-132-3p抑制lps诱导的ALI。因此，Arid2-IR和miR-132-3p可能相互作用参与了lps诱导的肺炎ALI。本研究旨在探讨Arid2-IR和miR-132-3p在肺炎ALI中的相互作用。材料和方法:从肺炎患者(n = 98)和健康对照(n = 98)中抽取血浆样本，检测循环Arid2-IR和miR-132-3p的表达。采用Pearson相关系数分析两者之间的相关性。通过过表达实验分析了它们在人支气管上皮细胞(HBEpC)中的串扰。应用MSP检测miR-132-3p基因的甲基化。采用2,5-二苯基- 2h -溴化四氮唑法测定细胞活力。结果:Arid2-IR在肺炎组中高度上调，miR-132-3p在肺炎组中表达水平较对照组降低。Arid2-IR和miR-132-3p在患者样本中呈负相关。Arid2-IR过表达降低了hbepc中miR-132-3p的表达水平，增加了miR-132-3p基因的甲基化。Arid2-IR抑制miR-132-3p在提高LPS诱导的hbepc活力中的作用。讨论与结论:Arid2-IR在肺炎中表达上调，可能通过增加miR-132-3p的甲基化而下调miR-132-3p，从而降低细胞活力，从而促进lps诱导的肺炎ALI。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Inhalation Toxicology 医学-毒理学

CiteScore

4.10

自引率

4.80%

发文量

审稿时长

6-12 weeks

期刊介绍： Inhalation Toxicology is a peer-reviewed publication providing a key forum for the latest accomplishments and advancements in concepts, approaches, and procedures presently being used to evaluate the health risk associated with airborne chemicals. The journal publishes original research, reviews, symposia, and workshop topics involving the respiratory system’s functions in health and disease, the pathogenesis and mechanism of injury, the extrapolation of animal data to humans, the effects of inhaled substances on extra-pulmonary systems, as well as reliable and innovative models for predicting human disease.