Low Endothelial Sheer Stress　― A Silent Killer ―

Abe, Shichiro; Nishino, Seiji; Sakuma, Masashi; Inoue, Teruo

doi:10.1253/circj.cj-19-0354

Cited by 2 publications

(2 citation statements)

References 13 publications

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“…Several studies have shown that OS could induce widespread gene expression alterations in ECS that might be involved in the progression of AS [8,[13][14][15]. Studies have demonstrated that vulnerable atherosclerotic plaques preferentially develop in regions with OS, and the fibrous cap was thinner, and the prevalence rates of thin-cap fibroatheroma (TCFA) were higher in the vascular segments with persistently OS than in other segments [7,16]. Although the close link between OS and AS plaque formation has been recognized, the intimate molecular mechanisms remain unclear.…”

Section: Introductionmentioning

confidence: 99%

Exploration of the Crucial Genes and Molecular Mechanisms Mediating Atherosclerosis and Abnormal Endothelial Shear Stress

et al. 2022

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Background. Abnormal endothelial shear stress (ESS) is a significant risk factor for atherosclerosis (AS); however, the genes and pathways between ESS and AS are poorly understood. Here, we screened hub genes and potential regulatory targets linked to the progression of AS induced by abnormal ESS. Methods. The microarray data of ESS and AS were downloaded from the Gene Expression Omnibus (GEO) database. The coexpression modules related to shear stress and AS were identified with weighted gene coexpression network analysis (WGCNA). Coexpression genes in modules obtained from GSE28829 and GSE160611 were considered as SET1. The results were validated in validation set by differential gene analysis. The limma package in R was used to identify differentially expressed genes (DEGs). The common DEGs of GSE100927 and GSE103672 were regarded as SET2. Next, Gene Ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis was conducted. Protein-protein interaction (PPI) enrichment analysis was assembled, and hub genes were identified using MCODE and ClueGO in Cytoscape. ROC curve analyses were conducted to assess the ability of common hub genes to distinguish samples of atherosclerotic plaque from normal arterial. The expression of common hub gene was verified in ox-LDL-induced foam cells and GSE41571. Results. We identified three gene modules (the blue, tan, and cyan modules) related to AS and three shear stress-related modules (the brown, red, and pink modules). A total of 129 genes in SET1 and 476 genes in SET2 were identified. CCRL2, LGALS9, and PLCB2 were identified as common hub genes and validated in the GSE100927, GSE28829, and GSE41571. ROC analysis indicates the expression of CCRL2, LGALS9, and PLCB2 could effectively distinguish the atherosclerotic plaque and normal arterial. The expression level of CCRL2, LGALS9, and PLCB2 increases with the accumulation of lipid increased. Conclusion. We identified CCRL2, LGALS9, and PLCB2 as key genes associated with abnormal ESS and AS and may provide potential prevention and treatment target of AS induced by abnormal ESS.

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Section: Introductionmentioning

confidence: 99%

Exploration of the Crucial Genes and Molecular Mechanisms Mediating Atherosclerosis and Abnormal Endothelial Shear Stress

et al. 2022

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“…Studies have demonstrated that vulnerable atherosclerotic plaques preferentially develop in regions with low ESS, and the brous cap was thinner and the prevalence rates of thin-cap broatheroma (TCFA) was higher in the vascular segments with persistently low EES than in other segments [7,12]. At the same time, higher ESS may lead to increased platelet aggregation, plaque erosion and plaque rupture [13,14].…”

Section: Introductionmentioning

confidence: 99%

Identification of Novel Hub Genes in Atherosclerosis Induced by Abnormal Endothelial Shear Stress via Bioinformatics Analysis

Zhu

Liu

Chen

et al. 2022

Preprint

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Background: Abnormal endothelial shear stress (ESS) is a significant risk factor for atherosclerosis (AS); however, the genes and pathways between ESS and AS are poorly understood. Here, we screened hub genes and potential regulatory targets linked to the progression of AS induced by abnormal ESS. Methods: GSE45225, GSE23289 and GSE43292 were downloaded from the Gene Expression Omnibus (GEO) database. The limma package in R was used to identify differentially expressed genes (DEGs). The common DEGs of GSE45225 and GSE43292 were regarded as low-ESS-AS related genes. Co-DEGs obtained from GSE23289 and GSE43292 were considered as high-ESS-AS related genes. Next, Gene Ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were conducted. Molecular interaction networks were assembled and their crucial genes were identified using Cytoscape. Our findings were also verified in GSE28829, GSE100927. Results: A total of 85 low-ESS-AS related genes and 118 high-ESS-AS related genes were identified. FBXO32, ICAM1 and TNFRSF1B were identified as key hub genes and validated in the GSE28829, GSE100927. ROC analysis indicates that FBXO32 (AUC=0.782), ICAM1 (AUC=0.822) and TNFRSF1B (AUC=0.801) could effectively distinguish the atherosclerotic plaque and normal arterial. Conclusion: We identified ICAM1, TNFRSF1B and FBXO32 as key genes associated with abnormal ESS and AS and may provide potential prevention and treatment target of AS induced by abnormal ESS.

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Low Endothelial Sheer Stress　― A Silent Killer ―

Cited by 2 publications

References 13 publications

Exploration of the Crucial Genes and Molecular Mechanisms Mediating Atherosclerosis and Abnormal Endothelial Shear Stress

Exploration of the Crucial Genes and Molecular Mechanisms Mediating Atherosclerosis and Abnormal Endothelial Shear Stress

Identification of Novel Hub Genes in Atherosclerosis Induced by Abnormal Endothelial Shear Stress via Bioinformatics Analysis

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Low Endothelial Sheer Stress ― A Silent Killer ―

Cited by 2 publications

References 13 publications

Exploration of the Crucial Genes and Molecular Mechanisms Mediating Atherosclerosis and Abnormal Endothelial Shear Stress

Exploration of the Crucial Genes and Molecular Mechanisms Mediating Atherosclerosis and Abnormal Endothelial Shear Stress

Identification of Novel Hub Genes in Atherosclerosis Induced by Abnormal Endothelial Shear Stress via Bioinformatics Analysis

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Low Endothelial Sheer Stress　― A Silent Killer ―