Analysis of differentially expressed circular RNAs in endothelial cells under impinging flow

Zheng, Hao; Li, Yiyun; Yu, Nianzu; Zhao, Yue; Hu, Si; Liu, Zheng; Li, Meihua

doi:10.1016/j.mcp.2020.101539

Cited by 4 publications

(3 citation statements)

References 37 publications

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“…It was revealed that most genes that were downregulated in MIA were mainly involved in inflammation, which is known to be critical for the pathogenesis of IA. This was similar to the results of Hao et al (24) and Huang et al (25). Inflammation of the arterial wall is one of the recognized mechanisms of IA (26).…”

Section: Discussionsupporting

confidence: 92%

Circular RNA expression profile in human primary multiple intracranial aneurysm

et al. 2021

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Primary multiple intracranial aneurysm (MIA) is a vascular disease that frequently leads to fatal vascular rupture and subarachnoid hemorrhage. However, the epigenetic regulation associated with MIA has remained largely elusive. Circular RNAs (circRNAs) serve important roles in cardiovascular diseases; however, their association with MIA has remained to be investigated. The present study initially aimed to explore novel mechanisms of MIA through examining circRNA expression profiles. Comprehensive circRNA expression profiles were detected by RNA sequencing (RNA-Seq) in human peripheral blood mononuclear cells. The RNA-Seq results were validated by reverse transcription-quantitative PCR. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses suggested the functions of these circRNAs. A competing endogenous RNA network was constructed to reveal the circRNA-microRNA-mRNA relationship. Among the 3,328 differentially expressed circRNAs between the MIA and matched control groups, 60 exhibited significant expression changes (|log2 fold change|≥2; P<0.05). Among these 60 circRNAs, 20 were upregulated, while the other 40 were downregulated. A number of downregulated circRNAs were involved in inflammation. The most significant KEGG pathway was ‘leukocyte transendothelial migration’. The circRNAs Homo sapiens (hsa)_circ_0135895, hsa_circ_0000682 and hsa_circ_0000690, which were also associated with the above-mentioned pathway, were indicated to be able to regulate protein tyrosine kinase 2, protein kinase Cβ and integrin subunit αL, respectively. To the best of our knowledge, the present study was the first to perform a circRNA sequencing analysis of MIA. The results specifically predicted the regulatory role of circRNAs in the pathogenesis of MIA. ‘Leukocyte transendothelial migration’ may be critical for the pathogenesis of MIA.

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Section: Discussionsupporting

confidence: 92%

Circular RNA expression profile in human primary multiple intracranial aneurysm

et al. 2021

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“…The T-Chamber System and Cell Culture In this research, a modified T-chamber was applied to generate impinging flow as previously described [10,[27][28][29][30]. WSS ranged from 18 to 36 dynes/cm 2 and WSSG from 0 to 140 dynes/cm 3 at a flow rate of 500 mL/min.…”

Section: Methodsmentioning

confidence: 99%

“…It is now generally accepted that endothelial cell (EC) dysfunction is a crucial factor and the first event in the formation of IA [5][6][7][8]. Arterial blood flow or impinging flow can create wall shear stress (WSS) in the vessel wall [9,10], which can lead to abnormal EC morphology and function [4,11]. This effect is particularly pronounced at bifurcation sites of intracranial arterial vessels, which are more prone to aneurysm formation [12].…”

Section: Introductionmentioning

confidence: 99%

HMGB1 Induced Oxidative Stress and Inflammation in Endothelial Cells Exposed to Impinging Flow

Zhu,

Zeng,

Tan

et al. 2023

Cerebrovasc Dis

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Background: Oxidative stress and inflammation contribute to many aspects of the pathological processes involved in intracranial aneurysm (IA). However, the underlying mechanism for inducing oxidative stress and inflammation under impinging flow remains unclear. Accumulating evidence has shown that High mobility group box-1 (HMGB1) is associated with oxidative stress-related chronic diseases and inflammatory responses. Therefore, we aimed to investigate whether HMGB1 is involved in oxidative stress and inflammatory responses in endothelial cells (ECs) exposed to impinging flow. Methods: We used a modified T-chamber to simulate the in vitro situation of human umbilical vein endothelial cells (HUVECs) subjected to impinging flow at the arterial bifurcation in order to analyze the effect of wall shear stress (WSS) on the ECs. To investigate the role of HMGB1 in this process, we transfected ECs with shRNA before conducting impinging flow experiments. Intracellular reactive oxygen species (ROS) were measured by flow cytometry, and malondialdehyde (MDA), glutathione (GSH), and superoxide dismutase (SOD) levels were measured to assess oxidative stress. Inflammation was assessed by measuring the mRNA expression levels of IL-1β, IL-6 and IL-8 using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). We also examined the cellular localisation of HMGB1 by immunofluorescence. Results: Exposure of HUVECs to WSS can increase the level of oxidative stress and inflammatory response. WSS increased the expression of HMGB1 in ECs and promoted the translocation of HMGB1 from cytosol to cytoplasm. When we knocked down HMGB1, the level of oxidative stress and inflammatory response caused by WSS in ECs decreased, suggesting that HMGB1 can mediate the oxidative stress and inflammatory response in HUVECs exposed to WSS. Conclusions：HMGB1 induced oxidative stress and inflammatory response in ECs exposed to Impinging Flow.

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