Mir-150-5p distinguishes acute pulmonary embolism, predicts the occurrence of pulmonary arterial hypertension, and regulates ox-LDL-induced endothelial cell injury

IF 2.7 3区 生物学
Yue Wu, Xin Sun, Guangqiang Cui, Shu Wang
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引用次数: 0

Abstract

Acute pulmonary embolism (APE) is a major type of venous thromboembolism (VTE) with a high risk of mortality and disability. There is a lack of biomarkers for APE to indicate deteriorating development and predict adverse outcomes. This study evaluated the significance of miR-150-5p in APE aiming to explore a novel potential biomarker for APE. The study enrolled APE (n = 137) and deep wein thrombosis (DVT, n = 67) patients and collected plasma samples from all study subjects. The expression of miR-150-5p was analyzed by PCR and its significance in screening APE and pulmonary arterial hypertension (PAH) was assessed by receiver operating curve (ROC) and logistic analyses. The study established oxidized low-density lipoprotein (ox-LDL)-induced human venous endothelial cells (HUVECs). Through cell transfection combined with cell counting kit-8 (CCK8), flow cytometry, and enzyme-linked immunosorbent assay (ELISA), the effect of miR-150-5p on ox-LDL-induced HUVEC injury was evaluated. Significant downregulation of miR-150-5p was observed in the plasma of APE patients compared with DVT patients (P < 0.0001). The plasma miR-150-5p levels in APE patients occurred PAH was much lower than in patients without PAH (P < 0.0001). Reducing miR-150-5p distinguished APE patients from DVT patients (AUC = 0.912) and was identified as a risk factor for the occurrence of PAH in APE patients (OR = 0.385, P = 0.010). In HUVECs, oxidized low-density lipoprotein (ox-LDL) caused inhibited cell proliferation, enhanced apoptosis, increased pro-inflammatory cytokines, reactive oxygen species (ROS), malondialdehyde (MDA), and decreased superoxide dismutase (SOD). Overexpressing miR-150-5p could promote proliferation, inhibit apoptosis, and alleviate inflammation and oxidative stress of ox-LDL-treated HUVECs. Downregulated plasma miR-150-5p served as a diagnostic biomarker for APE and predicted the predisposition of PAH in APE patients. Overexpressing miR-150-5p could alleviate ox-LDL-induced endothelial cell injury in HUVECs.
Mir-150-5p 可区分急性肺栓塞、预测肺动脉高压的发生并调节氧化-LDL 诱导的内皮细胞损伤
急性肺栓塞(APE)是静脉血栓栓塞症(VTE)的一种主要类型,具有很高的致死和致残风险。目前还缺乏表明 APE 发展恶化和预测不良后果的生物标志物。本研究评估了 miR-150-5p 在 APE 中的重要性,旨在探索 APE 的新型潜在生物标志物。研究招募了 APE(137 人)和深静脉血栓形成(67 人)患者,并收集了所有研究对象的血浆样本。通过 PCR 分析了 miR-150-5p 的表达,并通过接收器操作曲线(ROC)和逻辑分析评估了其在筛查 APE 和肺动脉高压(PAH)中的意义。该研究建立了氧化低密度脂蛋白(ox-LDL)诱导的人静脉内皮细胞(HUVECs)。通过细胞转染结合细胞计数试剂盒-8(CCK8)、流式细胞术和酶联免疫吸附试验(ELISA),评估了 miR-150-5p 对 ox-LDL 诱导的 HUVEC 损伤的影响。与深静脉血栓患者相比,在 APE 患者血浆中观察到 miR-150-5p 明显下调(P < 0.0001)。发生 PAH 的 APE 患者的血浆 miR-150-5p 水平远低于未发生 PAH 的患者(P < 0.0001)。降低的 miR-150-5p 可将 APE 患者与深静脉血栓患者区分开来(AUC = 0.912),并被确定为 APE 患者发生 PAH 的危险因素(OR = 0.385,P = 0.010)。在 HUVECs 中,氧化低密度脂蛋白(ox-LDL)会抑制细胞增殖、促进细胞凋亡、增加促炎细胞因子、活性氧(ROS)、丙二醛(MDA)和减少超氧化物歧化酶(SOD)。过表达 miR-150-5p 可促进氧化-LDL 处理的 HUVEC 的增殖、抑制凋亡、缓解炎症和氧化应激。下调的血浆 miR-150-5p 可作为 APE 的诊断生物标志物,并预测 APE 患者的 PAH 易感性。过表达 miR-150-5p 可减轻氧化-LDL 诱导的 HUVECs 内皮细胞损伤。
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
Hereditas
Hereditas Biochemistry, Genetics and Molecular Biology-Genetics
CiteScore
3.80
自引率
3.70%
发文量
0
期刊介绍: For almost a century, Hereditas has published original cutting-edge research and reviews. As the Official journal of the Mendelian Society of Lund, the journal welcomes research from across all areas of genetics and genomics. Topics of interest include human and medical genetics, animal and plant genetics, microbial genetics, agriculture and bioinformatics.
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