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Brain endothelial cells with inflammatory signature in CCM disease in hypoxia and normoxia conditions (HUVECs)

ABSTRACT: Brain endothelial cells with inflammatory signature in CCM disease in hypoxia and normoxia conditions (HUVECs)

PROVIDER: PRJNA1219536 | ENA |

REPOSITORIES: ENA

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			Action	DRS
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	SRR32238537_1.fastq.gz	Fastqsanger.gz
	SRR32238537_2.fastq.gz	Fastqsanger.gz
	SRR32238541_1.fastq.gz	Fastqsanger.gz
	SRR32238541_2.fastq.gz	Fastqsanger.gz

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Silencing KRIT1 Partially Reverses the Effects of Disturbed Flow on the Endothelial Cell Transcriptome

Project description:Endothelial cells respond to forces generated by laminar blood flow with changes in vasodilation, anticoagulant, fibrinolytic, or anti-inflammatory functions which preserve vessel patency. These responses to flow are primarily mediated by the elevation of transcription factors Krüppel-like factors 2 and 4 (KLF2 and KLF4). Notably, turbulent flow patterns, which predispose to atherosclerosis, significantly reduce the endothelial expression of KLF2 and KLF4 and reulting changes in the transcriptome that exacerbate inflammation and thrombosis. The CCM complex, comprising KRIT1, CCM2, and CCM3 suppress expression of KLF2 and KLF4. Loss of function of the CCM complex has recently been suggested to protect from coronary atherosclerosis in humans. We thus hypothesized that silencing of KRIT1, the central scaffold of the CCM complex, can normalize the effects of turbulent flow on the human endothelial transcriptome. We conducted bulk RNA sequencing (RNA-seq) on human umbilical vein endothelial cells (HUVECs) after silencing KRIT1 expression using specific siRNAs. The endothelial cells were exposed to pulsatile shear stress (laminar flow), oscillatory shear stress (disturbed flow), or no flow for 24 hours.

2025-05-29 | GSE288811 | GEO

Genome-wide analysis of mechanosensitive genes using in vivo model of mouse carotid artery endothelium exposed to disturbed flow

Project description:Recently, we have shown that disturbed flow caused by partial ligation of mouse carotid artery rapidly induces endothelial dysfunction and atherosclerosis within two weeks. To understand the molecular mechanisms by which disturbed flow induces atherosclerosis, we carried out genome-wide microarray study using endothelial RNAs isolated from the flow-disturbed left and the contralateral right common carotid artery (LCA and RCA) in C57BL/6 mice. Total intimal RNAs were obtained from LCA and RCA at 12hr and at 48hr post-ligation. Intimal RNAs from three LCAs or RCAs were pooled to obtain ~30ng total RNA.

2011-03-10 | E-GEOD-20741 | biostudies-arrayexpress

Genome-wide analysis of mechanosensitive genes using in vivo model of mouse carotid artery endothelium exposed to disturbed flow

2011-03-10 | GSE20741 | GEO

Disruption of the Novel Nested Gene Aff3ir Mediates Disturbed Flow-Induced Atherosclerosis in Mice

Project description:Disturbed shear stress-induced endothelial atherogenic responses are pivotal in the initiation and progression of atherosclerosis, contributing to the uneven distribution of atherosclerotic lesions. This study investigates the role of Aff3ir-ORF2, a novel nested gene variant, in disturbed flow-induced endothelial cell activation and atherosclerosis.

2025-04-14 | GSE286206 | GEO

Role of Fibulin-V (FibV) in disturbed flow induced arterial stiffening and atherosclerosis

Project description:The mechanisms of arterial stiffness (independent cardiovascular risk factor) are not well understood. Here, we investigated the role of Fibulin V in arterial stiffness and remodeling in response to disturbed blood flow.

2024-10-01 | GSE222583 | GEO

Disturbed flow promotes arterial stiffening through thrombospondin-1 (TSP-1) signaling pathways

Project description:Arterial stiffness is a prevalent, independent cardiovascular risk factor, but the underlying mechanisms are not well understood. Wall shear stress and shear-sensitive genes may promote arterial stiffening through clinically important signaling pathways. Our goal was to identify how disturbed blood flow leads to arterial stiffness using the mouse partial carotid ligation model. Here we used our in vivo partial carotid ligation model to induce d-flow in the LCA while the contralateral RCA continues to experience stable laminar flow using the C57BL/6x129SvEv mice, TSP-1 knockout (KO), and C57Bl/6J mice. We compared these to aged (80 week) mice which had increased arterial stiffness due to aging. Changes in gene expression were identified using microarrays that were performed on the endothelial-enriched RNA isolated from the carotids exposed to stable flow (RCA) and compared to disturbed flow (LCA). Arterial stiffness was determined ex vivo by biaxial mechanical testing and in vivo by ultrasound techniques. Myointimal hyperplasia and immunohistochemistry were performed in sectioned carotid arteries. In vitro testing of signaling pathways utilized oscillatory and laminar wall shear stress. Human arteries were tested ex vivo to validate critical results found in the animal model.

2017-09-01 | GSE87199 | GEO

Transcription profiling of pig aortic endothelium taken from regions of disturbed and undisturbed flow

Project description:This study investigates the role of endothelial cell (EC) gene expression in the focal origin of atherosclerosis, particularly in response to local hemodynamics. Differential gene expression was profiled in EC isolated from athero-susceptible and athero-protected regions of the normal pig aorta. Specifically, a region of disturbed flow (DF, the inner aortic arch) was compared to a region of undisturbed flow (UF, descending thoracic aorta). Linearly amplified RNA was used to screen nylon filter arrays of 13,824 human cDNAs.

2006-07-21 | E-CBIL-17 | biostudies-arrayexpress

Identification of novel mechanosensitive genes differentially regulated at 48 h timepoint in vivo using mouse carotid artery endothelium exposed to disturbed blood flow

2014-01-13 | GSE52243 | GEO

Identification of novel mechanosensitive genes differentially regulated at 48 h timepoint in vivo using mouse carotid artery endothelium exposed to disturbed blood flow

Project description:Recently, we showed that disturbed ﬂow caused by a partial ligation ofmouse carotid artery rapidly induces atherosclerosis. Analysis of mechanosenstive microRNA in the mouse carotid endothelium. In this study, we examined the microRNAs that respond differentially to blood flow pattern in the mouse carotid endothelium. We surgically induced disturbed blood flow in the left common carotid cartery (LCA) using partial carotid ligation surgery while the right carotid artery was left undisturbed. The hypothesis tested here is that turbulent or disturbed blood flow across the left carotid artery endothelium will affect endothelial genes and microRNAS. Identifying flow-sensitive microRNAs will provide important information about how endothelium responds to d-flow and regulates endothelial function and progression of atherosclerosis. Deter- mining the functional importance of these novel mechanosensitive microRNAS may provide important insights into understanding vascular biology and atherosclerosis. We used 6- to 8-week-old male C57Bl/6 mice (The Jackson Laboratory) according to the approved Institutional Animal Care and Use Committee protocol by Emory University. Mice were subjected to partial carotid ligation surgery under anesthesia. Brieﬂy, 3 of 4 caudal branches of LCA (left external carotid, internal carotid, and occipital artery) were ligated with 6-0 silk suture, although the superior thyroid artery was left intact. Development of low and oscillatory blood flow in the Left Carotid Artery of each mouse was determined by ultrasound measurements.

2014-01-13 | E-GEOD-52243 | biostudies-arrayexpress

Changes in miR expression profile carotid plaques induced by acutely induced flow disturbances in apoe-/- mice on a high fat diet.

Project description:Atherosclerosis is causally related to disturbed flow through low and oscillatory shear stress. In order to study the miR expression profile in atherosclerotic plaques induced by disturbed flow, partial ligation of the carotid artery was performed. This procedure results acutely in severly reduced blood flow and in stenotic lesion formation within 6 weeks in apoe-/- mice on a high fat diet. We compared the miR expression profile in partially ligated left carotid arteries with the untreated right carotid artery to identify miRs which are involved in plaque formation through flow disturbances. The left carotid arteries of 6 female apoe-/- mice (6-8 weeks) were partially ligated (i.e. the external and internal carotid artery as well as the occipital artery were occluded; blood flow out of the common carotid artery occurs mainly through the superior thyroid artery). Following partial ligation the animals were fed a high fat diet for 6 weeks. Total RNA was isolated from partially ligated left carotid arteries and untreated right carotid arteries (control). MiRs expression profile of the partially ligated carotid arteries were compared with the control group. Biological replicates: 6 per group. One replicate per array.

2012-12-26 | E-GEOD-26555 | biostudies-arrayexpress

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