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Histone Modifications and Chromatin Accessibility in Endothelial Cells under Shear Stress

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE128391 | GEO | 2020/03/11

REPOSITORIES: GEO

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Histone Modifications and Chromatin Accessibility in Endothelial Cells under Shear Stress (ATAC-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 | GSE128390 | GEO

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

2020-03-11 | GSE128389 | GEO

Histone Modifications and Chromatin Accessibility in Endothelial Cells under Shear Stress

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

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-05-28 | GSE152900 | GEO

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)

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

| PRJNA527305 | ENA

Fluid shear stress-modulated chromatin accessibility reveals the mechano-dependency of endothelial SMAD1/5-mediated gene transcription.

Project description:Bone morphogenetic protein (BMP) signaling and fluid shear stress (FSS) mediate complementary functions in vascular homeostasis and disease development. It remains to be shown whether altered chromatin accessibility downstream of BMP and FSS offers a crosstalk level to explain changes in SMAD-dependent transcription. Here, we employed ATAC-seq to analyze arterial endothelial cells stimulated with BMP9 and/or FSS. We found that BMP9-sensitive regions harbor non-palindromic GC-rich SMAD-binding elements (GGCTCC) and 69.7% of these regions become BMP-insensitive in the presence of FSS. While GATA and KLF transcription factor (TF) motifs are unique to BMP9- and FSS-sensitive regions, respectively, SOX motifs are common to both. Finally, we show that both SOX(13/18) and GATA(2/3/6) family members are directly upregulated by SMAD1/5. These findings highlight the mechano-dependency of SMAD-signaling by a sequential mechanism of first elevated pioneer TF expression, allowing subsequent chromatin opening to eventually providing accessibility to novel SMAD binding sites.

| S-EPMC10481294 | biostudies-literature

Cold stress induces enhanced chromatin accessibility and bivalent histone modifications H3K4me3 and H3K27me3 of active genes in potato.

Project description:BackgroundCold stress can greatly affect plant growth and development. Plants have developed special systems to respond to and tolerate cold stress. While plant scientists have discovered numerous genes involved in responses to cold stress, few studies have been dedicated to investigation of genome-wide chromatin dynamics induced by cold or other abiotic stresses.ResultsGenomic regions containing active cis-regulatory DNA elements can be identified as DNase I hypersensitive sites (DHSs). We develop high-resolution DHS maps in potato (Solanum tuberosum) using chromatin isolated from tubers stored under room (22?°C) and cold (4?°C) conditions. We find that cold stress induces a large number of DHSs enriched in genic regions which are frequently associated with differential gene expression in response to temperature variation. Surprisingly, active genes show enhanced chromatin accessibility upon cold stress. A large number of active genes in cold-stored tubers are associated with the bivalent H3K4me3-H3K27me3 mark in gene body regions. Interestingly, upregulated genes associated with the bivalent mark are involved in stress response, whereas downregulated genes with the bivalent mark are involved in developmental processes. In addition, we observe that the bivalent mark-associated genes are more accessible than others upon cold stress.ConclusionsCollectively, our results suggest that cold stress induces enhanced chromatin accessibility and bivalent histone modifications of active genes. We hypothesize that in cold-stored tubers, the bivalent H3K4me3-H3K27me3 mark represents a distinct chromatin environment with greater accessibility, which may facilitate the access of regulatory proteins required for gene upregulation or downregulation in response to cold stress.

| S-EPMC6580510 | biostudies-literature

Differential analysis of chromatin accessibility and histone modifications for predicting mouse developmental enhancers.

Project description:Enhancers are distal cis-regulatory elements that modulate gene expression. They are depleted of nucleosomes and enriched in specific histone modifications; thus, calling DNase-seq and histone mark ChIP-seq peaks can predict enhancers. We evaluated nine peak-calling algorithms for predicting enhancers validated by transgenic mouse assays. DNase and H3K27ac peaks were consistently more predictive than H3K4me1/2/3 and H3K9ac peaks. DFilter and Hotspot2 were the best DNase peak callers, while HOMER, MUSIC, MACS2, DFilter and F-seq were the best H3K27ac peak callers. We observed that the differential DNase or H3K27ac signals between two distant tissues increased the area under the precision-recall curve (PR-AUC) of DNase peaks by 17.5-166.7% and that of H3K27ac peaks by 7.1-22.2%. We further improved this differential signal method using multiple contrast tissues. Evaluated using a blind test, the differential H3K27ac signal method substantially improved PR-AUC from 0.48 to 0.75 for predicting heart enhancers. We further validated our approach using postnatal retina and cerebral cortex enhancers identified by massively parallel reporter assays, and observed improvements for both tissues. In summary, we compared nine peak callers and devised a superior method for predicting tissue-specific mouse developmental enhancers by reranking the called peaks.

| S-EPMC6265487 | biostudies-literature

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

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