Mus musculus strain:C57BL6
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA646233 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13959211_1.fastq.gz | Fastqsanger.gz | |||
| SRR13959211_2.fastq.gz | Fastqsanger.gz | |||
| SRR13959212_1.fastq.gz | Fastqsanger.gz | |||
| SRR13959212_2.fastq.gz | Fastqsanger.gz | |||
| SRR13959213_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 28 |
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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.
2011-03-10 | GSE20741 | GEO
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
Project description:Atherosclerosis, which develops in the inner layer of arteries, is the major cause of myocardial infarction and stroke. Atherosclerotic plaques develop preferentially in arterial regions exposed to disturbed blood flow, such as vessel curvatures, bifurcations and branching points, where endothelial cells develop an inflammatory phenotype. How disturbed flow induces endothelial cell inflammation is incompletely understood. We show here that histone H3.3 phosphorylation at serine 31 (H3.3S31) plays a critical role in disturbed flow-induced endothelial inflammation, as it allows the rapid induction of FOS and FOSB, which are required for disturbed flow-induced inflammatory gene expression. We identified protein kinase N1 (PKN1) as the kinase responsible for disturbed flow-induced H3.3S31 phosphorylation. PKN1 becomes activated by disturbed flow in an integrin a5b1-dependent manner and then translocates to the cell nucleus. We found that PKN1 is also involved in the phosphorylation of the AP-1 transcription factor JUN. Mice with endothelium-specific loss of PKN1 or endothelial expression of S31 phosphorylation-deficient mutants of H.3.3 show reduced endothelial inflammation and disturbed flow-induced vascular remodeling in vitro and in vivo. Our data identify a novel mechanism of H3.3S31 phosphorylation which may serve as a target for preventive and therapeutic anti-atherosclerotic strategies.
2024-11-26 | GSE261755 | GEO
Project description:Atherosclerosis, which develops in the inner layer of arteries, is the major cause of myocardial infarction and stroke. Atherosclerotic plaques develop preferentially in arterial regions exposed to disturbed blood flow, such as vessel curvatures, bifurcations and branching points, where endothelial cells develop an inflammatory phenotype. How disturbed flow induces endothelial cell inflammation is incompletely understood. We show here that histone H3.3 phosphorylation at serine 31 (H3.3S31) plays a critical role in disturbed flow-induced endothelial inflammation, as it allows the rapid induction of FOS and FOSB, which are required for disturbed flow-induced inflammatory gene expression. We identified protein kinase N1 (PKN1) as the kinase responsible for disturbed flow-induced H3.3S31 phosphorylation. PKN1 becomes activated by disturbed flow in an integrin a5b1-dependent manner and then translocates to the cell nucleus. We found that PKN1 is also involved in the phosphorylation of the AP-1 transcription factor JUN. Mice with endothelium-specific loss of PKN1 or endothelial expression of S31 phosphorylation-deficient mutants of H.3.3 show reduced endothelial inflammation and disturbed flow-induced vascular remodeling in vitro and in vivo. Our data identify a novel mechanism of H3.3S31 phosphorylation which may serve as a target for preventive and therapeutic anti-atherosclerotic strategies.
2024-11-26 | GSE261754 | GEO
Project description:Atherosclerosis, which develops in the inner layer of arteries, is the major cause of myocardial infarction and stroke. Atherosclerotic plaques develop preferentially in arterial regions exposed to disturbed blood flow, such as vessel curvatures, bifurcations and branching points, where endothelial cells develop an inflammatory phenotype. How disturbed flow induces endothelial cell inflammation is incompletely understood. We show here that histone H3.3 phosphorylation at serine 31 (H3.3S31) plays a critical role in disturbed flow-induced endothelial inflammation, as it allows the rapid induction of FOS and FOSB, which are required for disturbed flow-induced inflammatory gene expression. We identified protein kinase N1 (PKN1) as the kinase responsible for disturbed flow-induced H3.3S31 phosphorylation. PKN1 becomes activated by disturbed flow in an integrin a5b1-dependent manner and then translocates to the cell nucleus. We found that PKN1 is also involved in the phosphorylation of the AP-1 transcription factor JUN. Mice with endothelium-specific loss of PKN1 or endothelial expression of S31 phosphorylation-deficient mutants of H.3.3 show reduced endothelial inflammation and disturbed flow-induced vascular remodeling in vitro and in vivo. Our data identify a novel mechanism of H3.3S31 phosphorylation which may serve as a target for preventive and therapeutic anti-atherosclerotic strategies.
2024-11-26 | GSE261753 | GEO
Project description:Atherosclerosis preferentially develops in susceptible regions of the arterial system that are defined by the regional vascular hemodynamics. Previous work in adult castrate male pigs revealed the coexistence of pro- and anti-atherosclerotic profiles in endothelial cell gene expression in disturbed flow regions of arteries in the absence of risk factors for atherogenesis. This study investigates the impact of gender, high fat/high cholesterol diet and regional hemodynamics on arterial endothelial cell gene expression profiles in sexually mature intact pigs.
2007-12-15 | E-CBIL-41 | biostudies-arrayexpress
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.
2014-01-13 | GSE52243 | GEO
Project description:The luminal surface of the endothelium is exposed to dynamic blood flow patterns that are known to affect endothelial cell phenotype. In this study, human aortic endothelial cells (HAECs) were exposed to unidirectional laminar flow (20 dynes/cm2) or disturbed flow (±4 dynes/cm2, 2 Hz) for 48 hrs and then subjected to RNA sequencing. The sequencing data was used to analyze changes in endothelial cell gene expression and pathways associated with lipid metabolism.
2024-07-01 | GSE266437 | GEO
Project description:Exposure of the arterial endothelium to low and disturbed flow is a risk factor for the erosion and rupture of atherosclerotic plaques and aneurysms. Circulating and locally produced proteins are known to contribute to an altered matrix composition at the site of lesions, and to contribute to inflammatory processes within the lesions by altering the sub-endothelial matrix. We have previously shown that immune-cell regulated alternative splicing of Fibronectin (FN) protects against flow-induced hemorrhage. Here, we perform quantitative proteomic analysis of enriched extracellular matrix preparations from murine carotid arteries exposed to low and disturbed flow in vivo and examine serum derived and endothelial cell contributions to the sub-endothelial matrix in vitro. Our results reveal the extent of the dynamic alterations in extracellular matrix composition in the acute response to low and disturbed flow, and show how changes in the splicing of FN, a common response in vascular inflammation and remodeling, affects matrix composition.
2022-02-15 | PXD012474 | Pride
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