CircSEC11A knockdown alleviates oxidative stress and apoptosis and promotes cell proliferation and angiogenesis by regulating miR-29a-3p/SEMA3A axis in OGD-induced human brain microvascular endothelial cells (HBMECs).

IF 2.1 4区医学 Q3 HEMATOLOGY

Clinical hemorheology and microcirculation Pub Date : 2023-01-01 DOI:10.3233/CH-221689

Ziying Zhou, Qian Hu, Hongmei Guo, Xijia Wang

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引用次数: 2

Abstract

Background: Circular RNA (circRNA) has been found to play an important role in the progression of many diseases, including ischemic stroke. However, the regulatory mechanism of circSEC11A in ischemic stroke progression need to further investigation.

Methods: Human brain microvascular endothelial cells (HBMECs) were stimulated by oxygen glucose deprivation (OGD). CircSEC11A, SEC11A mRNA and miR (microRNA)-29a-3p were quantified by quantitative real-time PCR (qRT-PCR). SEMA3A, BAX and BCL2 protein level was quantified by western blot. Oxidative stress, cell proliferation, angiogenesis and apoptosis abilities were gauged by oxidative stress assay kit, 5-Ethynyl-2'-Deoxyuridine (EdU) staining, tube formation assay and flow cytometry assays, respectively. Direct relationship between miR-29a-3p and circSEC11A or SEMA3A was validated by dual-luciferase reporter assay, RIP assay and RNA pull-down assay.

Results: CircSEC11A was upregulated in OGD-induced HBMECs. OGD promoted the oxidative stress and apoptosis and inhibited cell proliferation and angiogenesis, while circSEC11A knockdown relieved the effects. CircSEC11A functioned as the sponge for miR-29a-3p, and miR-29a-3p inhibitor reversed the effects of si-circSEC11A on OGD-induced HBMECs oxidative injuries. Moreover, SEMA3A served as the target gene of miR-29a-3p. MiR-29a-3p inhibition ameliorated OGD-induced HBMECs oxidative injuries, while SEMA3A overexpression rescued the impacts of miR-29a-3p mimic.

Conclusion: CircSEC11A promoted the malignant progression in OGD-induced HBMECs through the mediation of miR-29a-3p/SEMA3A axis. This study has provided the new insight into the underlying application of circSEC11A in cell model of ischemic stroke.

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CircSEC11A敲低可通过调控miR-29a-3p/SEMA3A轴，缓解ogd诱导的人脑微血管内皮细胞(HBMECs)的氧化应激和凋亡，促进细胞增殖和血管生成。

背景:环状RNA (circRNA)已被发现在包括缺血性中风在内的许多疾病的进展中发挥重要作用。然而，circSEC11A在缺血性脑卒中进展中的调控机制有待进一步研究。方法:采用氧葡萄糖剥夺法(OGD)刺激人脑微血管内皮细胞(HBMECs)。采用实时荧光定量PCR (qRT-PCR)检测CircSEC11A、SEC11A mRNA和miR (microRNA)-29a-3p。western blot检测SEMA3A、BAX、BCL2蛋白水平。分别采用氧化应激检测试剂盒、5-乙基-2′-脱氧尿苷(EdU)染色、成管实验和流式细胞术检测氧化应激、细胞增殖、血管生成和凋亡能力。通过双荧光素酶报告基因实验、RIP实验和RNA下拉实验验证miR-29a-3p与circSEC11A或SEMA3A之间的直接关系。结果:CircSEC11A在ogd诱导的hbmec中表达上调。OGD促进氧化应激和细胞凋亡，抑制细胞增殖和血管生成，而敲低circSEC11A则缓解了这一作用。CircSEC11A作为miR-29a-3p的海绵，miR-29a-3p抑制剂逆转了si-circSEC11A对ogd诱导的hbmec氧化损伤的作用。此外，SEMA3A作为miR-29a-3p的靶基因。MiR-29a-3p抑制可改善ogd诱导的hbmec氧化损伤，而SEMA3A过表达可挽救MiR-29a-3p模拟物的影响。结论:CircSEC11A通过miR-29a-3p/SEMA3A轴介导ogd诱导的hbmec的恶性进展。本研究为circSEC11A在缺血性脑卒中细胞模型中的潜在应用提供了新的见解。

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

Clinical hemorheology and microcirculation 医学-外周血管病

CiteScore

4.30

自引率

33.30%

发文量

170

期刊介绍： Clinical Hemorheology and Microcirculation, a peer-reviewed international scientific journal, serves as an aid to understanding the flow properties of blood and the relationship to normal and abnormal physiology. The rapidly expanding science of hemorheology concerns blood, its components and the blood vessels with which blood interacts. It includes perihemorheology, i.e., the rheology of fluid and structures in the perivascular and interstitial spaces as well as the lymphatic system. The clinical aspects include pathogenesis, symptomatology and diagnostic methods, and the fields of prophylaxis and therapy in all branches of medicine and surgery, pharmacology and drug research. The endeavour of the Editors-in-Chief and publishers of Clinical Hemorheology and Microcirculation is to bring together contributions from those working in various fields related to blood flow all over the world. The editors of Clinical Hemorheology and Microcirculation are from those countries in Europe, Asia, Australia and America where appreciable work in clinical hemorheology and microcirculation is being carried out. Each editor takes responsibility to decide on the acceptance of a manuscript. He is required to have the manuscript appraised by two referees and may be one of them himself. The executive editorial office, to which the manuscripts have been submitted, is responsible for rapid handling of the reviewing process. Clinical Hemorheology and Microcirculation accepts original papers, brief communications, mini-reports and letters to the Editors-in-Chief. Review articles, providing general views and new insights into related subjects, are regularly invited by the Editors-in-Chief. Proceedings of international and national conferences on clinical hemorheology (in original form or as abstracts) complete the range of editorial features.