Circulating microvesicles miR139-3p from bronchopulmonary dysplasia aggravates pulmonary vascular simplification by targeting 4E binding protein 1

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC ACS Applied Electronic Materials Pub Date : 2024-02-22 DOI:10.1002/jgm.3675
Linchao Yu, Rui He, Chan Liu, Yuan Shi, Daoxin Wang
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Abstract

Background

Microvesicles (MVs) play a crucial role in bronchopulmonary dysplasia (BPD). There are many MVs in circulating plasma, and they are in direct contact with lung endothelial cells. However, the molecular mechanism and causative effect of circulating MVs on BPD remain unclear.

Methods

Clinical plasma samples were collected, circulating MVs were isolated, and microRNA (miRNA) sequencing was performed. The BPD model was established, and different MVs were administered. Alveoli and pulmonary vessels were examined by hematoxylin–eosin staining, and body weight and length were measured. In vitro, gene expression was disrupted by miRNA mimics, miRNA inhibitors or plasmid transfection. Cell proliferation and protein expression were detected by cell scratch assay, accurate 5-ethynyl-2-deoxyuridine test, western blotting, or immunofluorescence assay.

Results

BPD-derived MVs further aggravated pulmonary vascular simplification, while circulating MVs from control mice mitigated pulmonary vascular simplification. Micro-RNA sequencing and independent sample verification revealed that miR139-3p, but not miR6125 or miR193b-3p, was the most critical effector molecule in MVs. Mechanism studies showed that eukaryotic translation initiation factor 4E binding protein 1 was the target gene for miR139-3p. In addition, we found that supplementation of miR139-3p inhibitor partially alleviated pulmonary vascular simplification.

Conclusions

These results indicate that circulating MVs are involved in forming BPD by carrying miR139-3p molecules and support miR139-3p inhibitors as a potential therapeutic strategy for alleviating pulmonary vascular simplification in BPD.

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来自支气管肺发育不良的循环微囊miR139-3p通过靶向4E结合蛋白1加重肺血管简化。
背景:微囊泡(MVs)在支气管肺发育不良(BPD)中起着至关重要的作用。循环血浆中有许多微泡,它们与肺内皮细胞直接接触。然而,循环中膜对 BPD 的分子机制和致病作用仍不清楚:方法:收集临床血浆样本,分离循环 MVs,并进行 microRNA(miRNA)测序。方法:收集临床血浆样本,分离循环中微粒体,并进行微RNA(miRNA)测序。用苏木精-伊红染色法检查肺泡和肺血管,并测量体重和身长。在体外,通过 miRNA 模拟物、miRNA 抑制剂或质粒转染破坏基因表达。细胞增殖和蛋白质表达通过细胞划痕试验、5-乙炔基-2-脱氧尿苷精确试验、Western印迹或免疫荧光试验进行检测:结果:BPD衍生的MV进一步加重了肺血管的简化,而来自对照组小鼠的循环MV减轻了肺血管的简化。微RNA测序和独立样本验证显示,miR139-3p,而不是miR6125或miR193b-3p,是MVs中最关键的效应分子。机制研究表明,真核翻译起始因子 4E 结合蛋白 1 是 miR139-3p 的靶基因。此外,我们发现补充 miR139-3p 抑制剂可部分缓解肺血管简化:这些结果表明,循环中膜通过携带 miR139-3p 分子参与了 BPD 的形成,并支持将 miR139-3p 抑制剂作为缓解 BPD 肺血管简化的潜在治疗策略。
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
CiteScore
7.20
自引率
4.30%
发文量
567
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