Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-cell transcriptome analysis of endothelial cell heterogeneity under laminar shear stress

ABSTRACT: Heterogeneity of endothelial cells that form the innermost layer of all vessels is critical for vascular sprouting and angiogenesis. After new vessels form, endothelial cell heterogeneity is believed to be gradually lost as vessels respond to flow-mediated signals, mature, remodel and become homeostatic. However, whether and at what level endothelial cell lost heterogeneity is poorly understood. Here we investigated heterogeneity change of endothelial cells under homeostatic laminar shear tress in comparison to static cultures.

ORGANISM(S): Homo sapiens

PROVIDER: GSE151867 | GEO | 2021/05/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcriptome analysis of the role of SMAD6 in mediating endothelial cell response to laminar shear stress by high throughput RNA sequencing

Project description:Laminar shear stress regulates blood vessel morphogenesis and subsequent quiescence, but how endothelial cells (EC) enact and maintain the vascular homeostasis required in most vessels for proper vessel function is poorly understood. SMAD6, a scaffold for several signaling pathways, is expressed in developing arteries and its expression is flow-regulated. We found that SMAD6 is essential for endothelial cell flow-mediated responses, and that it functions downstream of the mechanosensor Notch1. Endothelial cells with reduced SMAD6 levels failed to align under stable laminar shear flow that promotes vascular homeostasis, while forced SMAD6 expression rescued misalignment induced by reduced Notch1 signaling. SMAD6-dependent homeostatic laminar flow required the Notch ligand Dll4 and Notch transcriptional activity. Mechanistically, neither the N-terminal nor the C-terminal domain of SMAD6 alone rescued flow alignment upon loss of Notch signaling. Endothelial cells with reduced Smad6 levels has compromised barrier function, and RNA profiling revealed upregulation of proliferation-associated genes and down regulation of junction-associated genes. Among junction-related genes affected by SMAD6 levels, the proto-cadherin PCDH12 was upregulated by homeostatic flow and required for proper flow-mediated endothelial cell alignment. Thus, SMAD6 is a critical integrator of flow-mediated signaling inputs downstream of Notch1, as vessels transition from an angiogenic to a homeostatic phenotype.

2021-03-29 | GSE147036 | 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

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

2009-05-23 | GSE13712 | GEO

Single-cell transcriptome analysis of endothelial cell heterogeneity under laminar shear stress

Project description:Single-cell transcriptome analysis of endothelial cell heterogeneity under laminar shear stress

| PRJNA637536 | ENA

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

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.

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

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

2021-05-28 | GSE152889 | GEO

Laminar shear stress regulated gene expression in HUVECs

Project description:To identify genes whose expression is regulated by laminar flow in HUVECs.

2022-04-07 | GSE167024 | GEO