Hsa_circ_0007765 在动脉粥样硬化中促进血小板衍生生长因子-BB 诱导的人主动脉血管平滑肌细胞的增殖和迁移。

IF 3.4 3区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS
Cardiovascular Toxicology Pub Date : 2024-10-01 Epub Date: 2024-08-10 DOI:10.1007/s12012-024-09899-6
Shengwei Ma, Haiyun Qian, Qian Zhou, Chengang Lei
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引用次数: 0

摘要

人体主动脉血管平滑肌细胞(HA-VSMCs)在动脉粥样硬化(AS)等血管疾病的发病机制中发挥着重要作用。据报道,环状 RNA(circRNA)可调控 HA-VSMC 的生物功能。因此,本研究旨在探讨 hsa_circRNA_102353 (circ_0007765) 在血小板衍生生长因子-BB(PDGF-BB)诱导的 HA-VSMCs 中的作用和机制。使用实时定量聚合酶链反应(RT-qPCR)测定了 Circ_0007765、microRNA-654-3p(miR-654-3p)和成纤维细胞生长因子受体底物 2(FRS2)的表达。细胞增殖能力、侵袭和迁移通过 3-(4,5-二甲基-2-噻唑基)-2,5-二苯基-2-H-溴化四氮唑(MTT)、5-乙炔基-2'-脱氧尿苷(EdU)、Transwell 和伤口愈合试验进行检测。采用 Western 印迹法评估 CyclinD1、MMP2 和 FRS2 蛋白水平。通过 Circinteractome 或 TargetScan 预测了 miR-654-3p 与 circ_0007765 或 FRS2 之间的结合,并通过双荧光素酶报告和 RNA 拉取试验进行了验证。PDGF-BB 可诱导 HA-VSMC 增殖、侵袭和迁移。经 PDGF-BB 处理的 HA-VSMC 中,Circ_0007765 和 FRS2 的表达水平升高,miR-654-3p 水平降低。此外,缺乏 circ_0007765 会阻碍 PDGF-BB 诱导的 HA-VSMC 体外增殖、侵袭和迁移。在分子水平上,circ_0007765 作为 miR-654-3p 的海绵,增加了 FRS2 的表达。我们的研究结果表明,circ_0007765通过吸附miR-654-3p提高了FRS2的表达,从而促进了PDGF-BB诱导的HA-VSMC的增殖和迁移,为强直性脊柱炎提供了一种可行的治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Hsa_circ_0007765 Promotes Platelet-Derived Growth Factor-BB-Induced Proliferation and Migration of Human Aortic Vascular Smooth Muscle Cells in Atherosclerosis.

Hsa_circ_0007765 Promotes Platelet-Derived Growth Factor-BB-Induced Proliferation and Migration of Human Aortic Vascular Smooth Muscle Cells in Atherosclerosis.

Human aortic vascular smooth muscle cells (HA-VSMCs) play vital roles in the pathogenesis of vascular diseases, including Atherosclerosis (AS). Circular RNAs (circRNAs) have been reported to regulate the biological functions of HA-VSMCs. Therefore, this study aimed to explore the role and mechanism of hsa_circRNA_102353 (circ_0007765) in platelet-derived growth factor-BB (PDGF-BB)-induced HA-VSMCs. Circ_0007765, microRNA-654-3p (miR-654-3p), and Fibroblast Growth Factor Receptor Substrate 2 (FRS2) expression were measured using real-time quantitative polymerase chain reaction (RT-qPCR). Cell proliferative ability, invasion, and migration were detected by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT), 5-ethynyl-2'-deoxyuridine (EdU), Transwell, and wound healing assays. CyclinD1, MMP2, and FRS2 protein levels were assessed using a Western blot assay. Binding between miR-654-3p and circ_0007765 or FRS2 was predicted by Circinteractome or TargetScan, and verified using dual-luciferase reporter and RNA pull-down assays. PDGF-BB induced HA-VSMC proliferation, invasion, and migration. Circ_0007765 and FRS2 expression levels were increased in PDGF-BB-treated HA-VSMCs, and the miR-654-3p level was reduced. Moreover, circ_0007765 absence hindered PDGF-BB-induced HA-VSMC proliferation, invasion, and migration in vitro. At the molecular level, circ_0007765 increased FRS2 expression by acting as a sponge for miR-654-3p. Our findings revealed that circ_0007765 boosted PDGF-BB-induced HA-VSMC proliferation and migration through elevating FRS2 expression via adsorbing miR-654-3p, providing a feasible therapeutic strategy for AS.

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来源期刊
Cardiovascular Toxicology
Cardiovascular Toxicology 医学-毒理学
CiteScore
6.60
自引率
3.10%
发文量
61
审稿时长
>12 weeks
期刊介绍: Cardiovascular Toxicology is the only journal dedicated to publishing contemporary issues, timely reviews, and experimental and clinical data on toxicological aspects of cardiovascular disease. CT publishes papers that will elucidate the effects, molecular mechanisms, and signaling pathways of environmental toxicants on the cardiovascular system. Also covered are the detrimental effects of new cardiovascular drugs, and cardiovascular effects of non-cardiovascular drugs, anti-cancer chemotherapy, and gene therapy. In addition, Cardiovascular Toxicology reports safety and toxicological data on new cardiovascular and non-cardiovascular drugs.
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