microRNA-130b-3p delivery by mesenchymal stem cells-derived exosomes confers protection on acute lung injury.

IF 3.3 4区医学 Q3 IMMUNOLOGY

Autoimmunity Pub Date : 2022-12-01 Epub Date: 2022-08-26 DOI:10.1080/08916934.2022.2094370

Xiaoxia Wang, Jifeng Feng, Huijun Dai, Jianlan Mo, Bijun Luo, Cheng Luo, Weikang Zhang, Linghui Pan

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引用次数: 4

Abstract

Objective: Researchers have investigated miR-130b-3p in lung disease pathology, such as lung fibrosis. The present study was performed to elucidate the miR-130b-3p-involved mechanism in acute lung injury (ALI) through delivery by mesenchymal stem cells-derived exosomes (MSCs-Exo).

Methods: ALI mouse models were induced via intratracheal administration of lipopolysaccharide (LPS) and treated with MSCs-Exo. Lung dry-wet (W/D) ratio, inflammatory factors in the bronchoalveolar lavage fluid, pathological damage and apoptosis in the lung tissues were analyzed. Expression levels of miR-130b-3p and TGFBR1 were measured in the mouse lung tissues, and the interaction between miR-130b-3p and TGFBR1 was studied.

Results: MSCs-Exo relieved LPS-induced ALI in mice by reducing lung W/D ratio and inflammatory response, and attenuating lung tissue pathological damage and reducing the alveolar cell apoptosis. miR-130b-3p delivery by MSCs-Exo reduced LPS-induced ALI in mice. TGFBR1 was determined to be a downstream target gene of miR-130b-3p. Inhibition of TGFBR1 could remit LPS-induced ALI in mice. The protection mediated by MSCs-Exo carrying miR-130b-3p could be rescued by elevating TGFBR1 expression.

Conclusion: miR-130b-3p delivery by MSCs-Exo confers protection on ALI in mice via the downregulation of TGFBR1.

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间充质干细胞来源的外泌体递送microRNA-130b-3p对急性肺损伤具有保护作用。

目的:研究miR-130b-3p在肺纤维化等肺部疾病病理中的作用。本研究旨在通过间充质干细胞来源的外泌体(msc - exo)递送阐明mir -130b-3p参与急性肺损伤(ALI)的机制。方法:采用脂多糖(LPS)气管内诱导ALI小鼠模型，并以MSCs-Exo处理。分析肺干湿比(W/D)、支气管肺泡灌洗液炎症因子、肺组织病理损伤及凋亡情况。检测miR-130b-3p和TGFBR1在小鼠肺组织中的表达水平，并研究miR-130b-3p与TGFBR1的相互作用。结果:MSCs-Exo通过降低肺W/D比和炎症反应，减轻肺组织病理损伤，减少肺泡细胞凋亡，减轻lps诱导的小鼠ALI。通过MSCs-Exo传递miR-130b-3p可减少lps诱导的小鼠ALI。TGFBR1被确定为miR-130b-3p的下游靶基因。抑制TGFBR1可缓解lps诱导的小鼠ALI。携带miR-130b-3p的msc - exo介导的保护作用可以通过提高TGFBR1的表达来恢复。结论:MSCs-Exo传递miR-130b-3p通过下调TGFBR1对小鼠ALI具有保护作用。

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

Autoimmunity 医学-免疫学

CiteScore

5.70

自引率

8.60%

发文量

审稿时长

6-12 weeks

期刊介绍： Autoimmunity is an international, peer reviewed journal that publishes articles on cell and molecular immunology, immunogenetics, molecular biology and autoimmunity. Current understanding of immunity and autoimmunity is being furthered by the progress in new molecular sciences that has recently been little short of spectacular. In addition to the basic elements and mechanisms of the immune system, Autoimmunity is interested in the cellular and molecular processes associated with systemic lupus erythematosus, rheumatoid arthritis, Sjogren syndrome, type I diabetes, multiple sclerosis and other systemic and organ-specific autoimmune disorders. The journal reflects the immunology areas where scientific progress is most rapid. It is a valuable tool to basic and translational researchers in cell biology, genetics and molecular biology of immunity and autoimmunity.