Department of Emergency Medicine, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, HaiKou City, Hainan Province, P.R. China.
Inhal Toxicol. 2022;34(11-12):297-303. doi: 10.1080/08958378.2022.2102699. Epub 2022 Sep 8.
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.
Plasma samples were obtained from patients with pneumonia ( = 98) and healthy controls ( = 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.
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.
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.
Arid2-IR 是一种长链非编码 RNA（lncRNA），可促进肾损伤，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 与 miR-132-3p 呈负相关，miR-132-3p 已知可抑制 LPS 诱导的 ALI。因此，Arid2-IR 和 miR-132-3p 可能相互作用，参与肺炎中 LPS 诱导的 ALI。本研究旨在探讨肺炎中 Arid2-IR 与 miR-132-3p 之间的相互作用。
收集肺炎患者（n=98）和健康对照者（n=98）的血浆样本，检测循环 Arid2-IR 和 miR-132-3p 的表达。采用 Pearson 相关系数分析它们之间的相关性。通过过表达试验分析它们在人支气管上皮细胞（HBEpC）中的相互作用。MSP 用于检测 miR-132-3p 基因的甲基化。采用 2,5-二苯基-2H-四唑溴盐法评价细胞活力。
肺炎组中 Arid2-IR 高表达，而肺炎组中 miR-132-3p 的表达水平较对照组降低。患者样本中 Arid2-IR 和 miR-132-3p 呈负相关。HBEpC 中转染 Arid2-IR 可降低 miR-132-3p 的表达水平并增加 miR-132-3p 基因的甲基化。Arid2-IR 抑制了 miR-132-3p 增加 LPS 诱导的 HBEpC 活力的作用。
肺炎中 Arid2-IR 上调，可能通过增加其甲基化降低 miR-132-3p 的表达，从而降低细胞活力，促进肺炎中 LPS 诱导的 ALI。
