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巨噬细胞来源的含 microRNA-19b-3p 的细胞外囊泡通过靶向 JAZF1 促进动脉粥样硬化的发展。

microRNA-19b-3p-containing extracellular vesicles derived from macrophages promote the development of atherosclerosis by targeting JAZF1.

机构信息

Department of Vascular Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, China.

Department of Vascular Surgery, Heilongjiang Provincial Hospital, Harbin, China.

出版信息

J Cell Mol Med. 2022 Jan;26(1):48-59. doi: 10.1111/jcmm.16938. Epub 2021 Dec 14.

DOI:10.1111/jcmm.16938
PMID:34910364
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8742201/
Abstract

Atherosclerosis has been regarded as a major contributor to cardiovascular disease. The role of extracellular vesicles (EVs) in the treatment of atherosclerosis has been increasingly reported. In this study, we set out to investigate the effect of macrophages-derived EVs (M-EVs) containing miR-19b-3p in the progression of atherosclerosis, with the involvement of JAZF1. Following isolation of EVs from macrophages, the M-EVs were induced with ox-low density lipoprotein (LDL) (ox-LDL-M-EVs), and co-cultured with vascular smooth muscle cells (VSMCs). RT-qPCR and western blot assay were performed to determine the expression of miR-19b-3p and JAZF1 in M-EVs and in VSMCs. Lentiviral infection was used to overexpress or knock down miR-19b-3p. EdU staining and scratch test were conducted to examine VSMC proliferation and migration. Dual-luciferase gene reporter assay was performed to examine the relationship between miR-19b-3p and JAZF1. In order to explore the role of ox-LDL-M-EVs carrying miR-19b-3p in atherosclerotic lesions in vivo, a mouse model of atherosclerosis was established through high-fat diet induction. M-EVs were internalized by VSMCs. VSMC migration and proliferation were promoted by ox-LDL-M-EVs. miR-19b-3p displayed upregulation in ox-LDL-M-EVs. miR-19b-3p was transferred by M-EVs into VSMCs, thereby promoting VSMC migration and proliferation. mir-19b-3p targeted JAZF1 to decrease its expression in VSMCs. Atherosclerosis lesions were aggravated by ox-LDL-M-EVs carrying miR-19b-3p in ApoE mice. Collectively, this study demonstrates that M-EVs containing miR-19b-3p accelerate migration and promotion of VSMCs through targeting JAZF1, which promotes the development of atherosclerosis.

摘要

动脉粥样硬化一直被认为是心血管疾病的主要诱因。细胞外囊泡（EVs）在动脉粥样硬化治疗中的作用已被越来越多地报道。在这项研究中，我们旨在研究载有 miR-19b-3p 的巨噬细胞衍生 EVs（M-EVs）在动脉粥样硬化进展中的作用，其中涉及 JAZF1。从巨噬细胞中分离出 EVs 后，用氧化低密度脂蛋白（ox-LDL）诱导 M-EVs（ox-LDL-M-EVs），并与血管平滑肌细胞（VSMCs）共培养。通过 RT-qPCR 和 Western blot 测定 M-EVs 和 VSMCs 中 miR-19b-3p 和 JAZF1 的表达。使用慢病毒感染过表达或敲低 miR-19b-3p。EdU 染色和划痕试验用于检测 VSMC 的增殖和迁移。双荧光素酶基因报告试验用于检测 miR-19b-3p 与 JAZF1 之间的关系。为了探讨携带 miR-19b-3p 的 ox-LDL-M-EVs 在体内动脉粥样硬化病变中的作用，通过高脂饮食诱导建立了动脉粥样硬化小鼠模型。M-EVs 被 VSMCs 内化。ox-LDL-M-EVs 促进了 VSMC 的迁移和增殖。ox-LDL-M-EVs 中 miR-19b-3p 上调。miR-19b-3p 通过 M-EVs 转移到 VSMCs 中，从而促进了 VSMC 的迁移和增殖。mir-19b-3p 靶向 JAZF1，降低了 VSMCs 中的表达。载有 miR-19b-3p 的 ox-LDL-M-EVs 加剧了 ApoE 小鼠的动脉粥样硬化病变。综上所述，这项研究表明，载有 miR-19b-3p 的 M-EVs 通过靶向 JAZF1 加速了 VSMCs 的迁移和增殖，从而促进了动脉粥样硬化的发展。

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