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Laminar shear stress inhibits inflammation by activating autophagy in human aortic endothelial cells through HMGB1 nuclear translocation

ABSTRACT: Laminar shear stress inhibits inflammation by activating autophagy in human aortic endothelial cells through HMGB1 nuclear translocation

PROVIDER: PRJNA821216 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18520202_1.fastq.gz	Fastqsanger.gz
	SRR18520202_2.fastq.gz	Fastqsanger.gz
	SRR18520203_1.fastq.gz	Fastqsanger.gz
	SRR18520203_2.fastq.gz	Fastqsanger.gz
	SRR18520204_1.fastq.gz	Fastqsanger.gz

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Laminar shear stress inhibits inflammation by activating autophagy in human aortic endothelial cells through HMGB1 nuclear translocation

Project description:Laminar shear stress (LSS) plays a variety of biological roles, one of which is regulation of gene expression in vascular endothelial cells. Prevention and treatment of atherosclerosis by targeting the inflammatory response in vascular endothelial cells has attracted much attention in recent years. In this study, we found that LSS could specifically inhibit the increased expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and matrix metallopeptidase-9 (MMP-9) caused by tumor necrosis factor-α (TNF-α) stimulation in an autophagy-dependent pathway in human aortic endothelial cells (HAECs) and human umbilical vein endothelial cells (HUVECs). Whole-transcriptome sequencing analysis revealed that erythropoietin-producing hepatocyte receptor B2 (EPHB2) was a key gene in response to LSS. Moreover, co-immunoprecipitation (co-IP) assay indicated that LSS could activate autophagy flux by enhancing the EPHB2-mediated nuclear translocation of high mobility group box-1 (HMGB1), which interacts with Beclin-1 (BECN1) and finally leads to autophagy in HAECs. We also found that overexpression of EPHB2 can activate autophagy and exert the same anti-inflammatory effect as LSS. Simultaneously, we identified a novel LSS-sensitive long non-coding RNA (lncRNA), LOC10798635, and constructed an LSS-related LOC107986345/miR-128-3p/EPHB2 regulatory axis. Further research revealed the inhibition of endothelial inflammatory by LSS depends on autophagy activation resulting from the nuclear translocation of HMGB1 via the LOC107986345/miR-128-3p/EPHB2 axis. In conclusion, our study demonstrates for the first time that LSS regulates the expression of EPHB2 in HAECs, and the LOC107986345/miR-128-3p/EPHB2 axis plays a vital role in atherosclerosis development.

2022-04-03 | GSE199709 | GEO

HUVECs cultured under normal or high laminar shear stress

Project description:Many studies have characterised the effect of normal laminar shear stress (LSS) on endothelial responses, however elevated shear stress, as would be experienced overlying a stenotic plaque, has not been studied in depth. Therefore we used transcriptomics and related functional analyses to compare cells exposed to laminar shear stress at 15 or 75 dynes/cm2 for 24 hours (LSS15-normal or LSS75-high shear stress). Human umbilical vein endothelial cells (HUVEC n=4 per flow condition from different batches of pooled donor HUVEC p2) were cultured for 24 hours on gelatin coated slides under laminar shear stress of either 15 dynes/cm2 or 75 dynes/cm2 (LSS15 or LSS75) to assess the effect of high shear stress on endothelial cells. Total RNA was obtained using Qiagen kit and array analysis performed by Service XS (Leiden, Netherlands).

2011-02-01 | E-GEOD-23289 | biostudies-arrayexpress

HUVECs cultured under normal or high laminar shear stress

2011-02-01 | GSE23289 | GEO

Transcription profiling by array of human young and senescent HUVECs under static and laminar shear stress conditions

Project description:Laminar shear stress due to constant blood flow is known to play a critical role in maintaining vascular health. In contrast, endothelial cell senescence appears to be closely associated with the incidence of vascular disorder. In an attempt to identify functional biomarkers for age-related vascular health/disease, the present study investigated differential gene expression of young and senescent human umbilical vein endothelial cells (HUVECs) under static and laminar shear stress. We used a cDNA microarray method to compare gene expression profiles of young and senescent HUVECs under static and laminar shear stress conditions. Experiment Overall Design: Senescent cells were prepared by continuous subculture in vitro, and a cone-and-plate device was used to impose laminar shear stress onto cells. Young and senescent cells were exposed to laminar shear stress or maintained under static conditions. Total mRNA was extracted and gene expression profiles were analyzed by cDNA microarray.

2009-06-01 | E-GEOD-13712 | biostudies-arrayexpress

Laminar shear stress inhibits inflammation by activating autophagy in human aortic endothelial cells through HMGB1 nuclear translocation.

Project description:Prevention and treatment of atherosclerosis (AS) by targeting the inflammatory response in vascular endothelial cells has attracted much attention in recent years. Laminar shear stress (LSS) has well-recognized anti-AS properties, however, the exact molecular mechanism remains unclear. In this study, we found that LSS could inhibit the increased expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and matrix metallopeptidase-9 (MMP-9) caused by TNF-α in an autophagy-dependent pathway in human aortic endothelial cells (HAECs) and human umbilical vein endothelial cells (HUVECs). Whole-transcriptome sequencing analysis revealed that erythropoietin-producing hepatocyte receptor B2 (EPHB2) was a key gene in response to LSS. Moreover, co-immunoprecipitation assay indicated that LSS could enhance the EPHB2-mediated nuclear translocation of high mobility group box-1 (HMGB1), which interacts with Beclin-1 (BECN1) and finally leads to autophagy. Simultaneously, we identified an LSS-sensitive long non-coding RNA (lncRNA), LOC10798635, and constructed an LSS-related LOC107986345/miR-128-3p/EPHB2 regulatory axis. Further research revealed the anti-inflammatory effect of LSS depends on autophagy activation resulting from the nuclear translocation of HMGB1 via the LOC107986345/miR-128-3p/EPHB2 axis. Our study demonstrates that LSS could regulate the expression of EPHB2 in HAECs, and the LOC107986345/miR-128-3p/EPHB2 axis plays a vital role in AS development.

| S-EPMC9076621 | biostudies-literature

Differential gene expression of young and senescent HUVECs under static and laminar shear stress conditions

2009-05-23 | GSE13712 | GEO

Genome-wide analysis of mechano-responsive gene expression of mesenchymal stem cells after laminar shear stress

Project description:Analysis of mechano-regulation of mesenchymal stem cell gene expression level. The hypothesis tested in the present study was that laminar shear stress influences the cytoskeleton arrangement and amount and then triggers seriers of cell metabolism and cellular functions. Results provide important information of the response of mesenchymal stem cell to laminar shear stress, such as specific mechano-responsive genes, up- or down-regulated specific anabolic/catabolic cellular functions.

2018-12-31 | GSE109180 | GEO

Comparison of aortic and aortic valve endothelial cells in static and shear environments

Project description:Porcine aortic and aortic valve endothelial cells were exposed to 20 dynes/cm2 steady laminar shear stress with static cultures serving as controls. Total RNA was hybridized to Agilent Human 1 cDNA arrays and processed using the Agilent Feature Extraction Software Keywords = aortic valve Keywords = endothelial Keywords = shear stress Keywords: other

2005-07-30 | GSE1637 | GEO

CircRNA profiling in laminar shear stress-treated human umbilical vein endothelial cells.

Project description:Laminar shear stress (LSS) suppresses endothelial inflammation and protects the arteries from atherosclerosis. Circular RNAs (circRNAs) are powerful regulators of vascular homeostasis and atherosclerosis; however, their roles in mediating the effects of LSS remain unexplored. To identify the changes in circRNA expression patterns after shear stress stimulation, we conducted circRNA microarray analysis using RNA extracted from HUVECs cultured for 24 h under static or LSS conditions.

2023-09-29 | GSE228636 | GEO

Laminar shear stress regulated gene expression in HUVECs

Project description:Laminar shear stress regulated gene expression in HUVECs

| PRJNA702756 | ENA