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Histone Modifications and Chromatin Accessibility in Endothelial Cells under Shear Stress

ABSTRACT: Histone Modifications and Chromatin Accessibility in Endothelial Cells under Shear Stress

PROVIDER: PRJNA527303 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8734970.fastq.gz	Fastqsanger.gz
	SRR8734980_1.fastq.gz	Fastqsanger.gz
	SRR8734980_2.fastq.gz	Fastqsanger.gz
	SRR8734971.fastq.gz	Fastqsanger.gz
	SRR8734981_1.fastq.gz	Fastqsanger.gz

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Histone Modifications and Chromatin Accessibility in Endothelial Cells under Shear Stress (ChIP-seq)

Project description:This data set reveals the changes of histone modifications and chromatin accessibility in human umbilical vein endothelial cells (HUVECs) under atheroprotective pulsatile shear (PS), atheroprone oscillatory shear (OS), or with KLF4 overexpression. Using ChIP-Seq, we defined the H3K27ac and H3K4me1 enrichment under PS and OS conditions. Using ATAC-seq, we identified the chromatin accessibility under KLF4 overexpression.

2020-03-11 | GSE128389 | GEO

Histone Modifications and Chromatin Accessibility in Endothelial Cells under Shear Stress (ATAC-seq)

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Histone Modifications and Chromatin Accessibility in Endothelial Cells under Shear Stress (ATAC-seq)

Project description:Histone Modifications and Chromatin Accessibility in Endothelial Cells under Shear Stress (ATAC-seq)

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Histone Modifications and Chromatin Accessibility in Endothelial Cells under Shear Stress (ChIP-seq)

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KLF4 Recruits SWI/SNF to Increase Chromatin Accessibility and Reprogram the Endothelial Enhancer Landscape under Laminar Shear Stress [ChIP-seq KLF & histone marks]

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KLF4 Recruits SWI/SNF to Increase Chromatin Accessibility and Reprogram the Endothelial Enhancer Landscape under Laminar Shear Stress

Project description:Physiologic laminar shear stress (LSS) induces an endothelial gene expression profile that is vasculo-protective. In this report, we delineate how LSS mediates changes in the epigenetic landscape to promote this beneficial response. We show that under LSS, KLF4 interacts with the SWI/SNF nucleosome remodeling complex to increase accessibility at enhancer sites that promote expression of homeostatic endothelial genes. By combining molecular and computational approaches we discovered enhancers that loop to promoters of known and novel KLF4- and LSS-responsive genes that stabilize endothelial cells and suppress inflammation, such as BMPR2 and DUSP5. By linking enhancers to genes that they regulate under physiologic LSS, our work establishes a foundation for interpreting how non-coding DNA variants in these regions might disrupt protective gene expression to influence vascular disease. AP-MS studies: For KLF gain-of-function, pulmonary artery endothelial cells (PAEC) were transduced with adenoviral vectors encoding a constitutively active mutant of MEK5 (caMEK5), or GFP as control. 90h post-transduction cells were lysed and AP was performed using antibodies targeting either KLF (sc166238, Santa Cruz Biotechnology) or FLAG (F7425, Millipore Sigma). Datafiles correspond to: GK: GFP-tranduced controls using anti-KLF antibodies for AP. GF: GFP-tranduced controls using anti-FLAG antibodies for AP. KK: caMEK5-transduced cells with anti-KLF antibodies for AP. KF: caMEK5-tranduced cells with anti-FLAG antibodies for AP.

2020-07-24 | MSV000085825 | MassIVE

Endothelial Response to Increased Shear Stress Frequency

Project description:Porcine endothelial cells were preconditioned by a basal level shear stress of 15 ± 15 dynes/cm2 at 1 Hz for 24 hours, and an acute increase in shear stress frequency (2 Hz) was then applied. The transcriptomics studies using microarray identified genes that were sensitive to the elevated shear frequency. keywords: adaptation, shear stress, frequency, microarray, gene expression Porcine endothelial cells were preconditioned by a basal level shear stress of 15 ± 15 dynes/cm2 at 1 Hz for 24 hours, and an acute increase in shear stress magnitude (2 Hz) was then applied. Gene expression at multiple time points was measured using microarray.

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KLF4 Recruits SWI/SNF to Increase Chromatin Accessibility and Reprogram the Endothelial Enhancer Landscape under Laminar Shear Stress [HiCHIP]

2021-05-28 | GSE153013 | GEO

KLF4 Recruits SWI/SNF to Increase Chromatin Accessibility and Reprogram the Endothelial Enhancer Landscape under Laminar Shear Stress [HiChIP2]

2022-04-02 | GSE199832 | GEO

Vascular-type heterogeneity is associated with differential gene expression profiles of endothelial cells under shear stress

Project description:Background: Endothelial cell (ECs) heterogeneity is an emerging area of research in EC biology. Veins, arteries, and microvascular endothelial cells, termed “vascular-type” heterogeneity in this report, have been shown to have heterogeneity in gene expression and function. In addition to this innate heterogeneity, we hypothesized that different vascular-type ECs would also demonstrate heterogeneity in their response to shear stress. Objectives: We interrogated whether vascular-type ECs would demonstrate variations in transcriptional expression patterns under shear stress. Methods: Human umbilical vein endothelial cells (HUVECs), human pulmonary arterial endothelial cells (HPAECs), and human microvascular endothelial cells (HMVECs) were commercially purchased and subjected to shear stress conditions of 0, 1, 4, and 10 dynes/cm2 of laminar shear stress. After exposure to shear stress, cells were analyzed for cellular alignment and RNA was extracted and evaluated via bulk RNA-sequencing (RNA-seq). Results: All ECs demonstrated significant changes in alignment under shear stress. Shear stress significantly affected the transcriptomes of ECs resulting in differentially expressed genes and pathways; while several genes were differentially expressed across all three vascular-types (44.2%), most differentially expressed genes were limited to 1 or 2 of the vascular-types. Hemostatic and thrombotic genes were found to have differential expression patterns under conditions of shear stress, and VWF demonstrated a pattern of vascular-type heterogeneity in response to shear stress. Conclusions: Shear stress causes changes in cellular alignment and transcriptional patterns in ECs that is dependent upon underlying vascular-type. Therefore, endothelial vascular-type heterogeneity can regulate response to shear stress, especially in hemostatic and thrombotic gene expression.

2025-07-23 | GSE294621 | GEO

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