Expression data from the carotid artery at 2 wks after Intimal injury
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ABSTRACT:
PROVIDER: PRJNA688710 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13330868_1.fastq.gz | Fastqsanger.gz | |||
| SRR13330868_2.fastq.gz | Fastqsanger.gz | |||
| SRR13330869_1.fastq.gz | Fastqsanger.gz | |||
| SRR13330869_2.fastq.gz | Fastqsanger.gz | |||
| SRR13330870_1.fastq.gz | Fastqsanger.gz |
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Project description:Injury of the arterial endothelial lamina, also called intimal injury, usually occurs after carotid endarterectomy, peripheral artery brachytherapy, stent placement for arterial occlusive disease and balloon dilatation surgeries. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process.
2021-03-23 | GSE164050 | GEO
Project description:The proliferation and remodeling of vascular smooth muscle cells (VSMCs) is an important pathological event in atherosclerosis and restenosis. Here we report that microRNA-132 (miR-132) blocks vascular smooth muscle cells (VSMC) proliferation by inhibiting the expression of LRRFIP1 [leucine-rich repeat (in Flightless 1) interacting protein-1]. MicroRNA microarray revealed that miR-132 was upregulated in the rat carotid artery after catheter injury, which was further confirmed by quantitative real-time RT-PCR. Transfection of an miR-132 mimic significantly inhibited the proliferation of VSMCs, whereas transfection of an miR-132 antagomir increased it. Bioinformatics showed that LRRFIP1 is a target candidate of miR-132. miR-132 down-regulated luciferase activity driven by a vector containing the 3’-untranslated region of Lrrfip1 in a sequence-specific manner. LRRFIP1 induced VSMC proliferation. Immunohistochemical analysis revealed that Lrrfip1 was clearly expressed along with the basal laminar area of smooth muscle, and its expression pattern was disrupted 7 days after arterial injury LRRFIP1 mRNA was decreased 14 days after injury. Delivery of miR-132 to rat carotid artery attenuated neointimal proliferation in carotid artery injury models. Our results suggest that miR-132 is a novel regulator of VSMC proliferation that represses neointimal formation by inhibiting LRRFIP1 expression. Balloon injury was induced in the carotid arteries of male Sprague–Dawley rats weighing approximately 250 g. Total RNA were extracted from the arterial sections after 10 days. MicroRNA profile of the sample was compared with non-injured control.
2013-04-23 | E-GEOD-45433 | biostudies-arrayexpress
Project description:Surgical interventions on blood vessels bear a risk for intimal hyperplasia and atherosclerosis as a consequence of injury. A specific feature of intimal hyperplasia is the loss of vascular smooth muscle cell (VSMC) differentiation gene expression. We hypothesized that immediate responses following injury induce vascular remodeling. To differentiate injury due to trauma, reperfusion and pressure changes we analyzed vascular responses to carotid artery bypass grafting in mice compared to transient ligation. As a control, the carotid artery was surgically laid open only. In both, bypass or ligation models, the inflammatory responses were transient, peaking after 6h, whereas the loss of VSMC differentiation gene expression persisted. Extended time kinetics showed that transient carotid artery ligation was sufficient to induce a persistent VSMC phenotype change throughout 28 days. Transient arterial ligation in ApoE knockout mice resulted in atherosclerosis in the transiently ligated vascular segment but not on the not-ligated contralateral side. The VSMC phenotype change could not be prevented by anti-TNF antibodies, Sorafenib, Cytosporone B or N-acetylcysteine treatment. Surgical interventions involving hypoxia/reperfusion are sufficient to induce VSMC phenotype changes and vascular remodeling. In situations of a perturbed lipid metabolism this bears the risk to precipitate atherosclerosis.
2018-09-06 | GSE119549 | GEO
Project description:The proliferation and remodeling of vascular smooth muscle cells (VSMCs) is an important pathological event in atherosclerosis and restenosis. Here we report that microRNA-132 (miR-132) blocks vascular smooth muscle cells (VSMC) proliferation by inhibiting the expression of LRRFIP1 [leucine-rich repeat (in Flightless 1) interacting protein-1]. MicroRNA microarray revealed that miR-132 was upregulated in the rat carotid artery after catheter injury, which was further confirmed by quantitative real-time RT-PCR. Transfection of an miR-132 mimic significantly inhibited the proliferation of VSMCs, whereas transfection of an miR-132 antagomir increased it. Bioinformatics showed that LRRFIP1 is a target candidate of miR-132. miR-132 down-regulated luciferase activity driven by a vector containing the 3’-untranslated region of Lrrfip1 in a sequence-specific manner. LRRFIP1 induced VSMC proliferation. Immunohistochemical analysis revealed that Lrrfip1 was clearly expressed along with the basal laminar area of smooth muscle, and its expression pattern was disrupted 7 days after arterial injury LRRFIP1 mRNA was decreased 14 days after injury. Delivery of miR-132 to rat carotid artery attenuated neointimal proliferation in carotid artery injury models. Our results suggest that miR-132 is a novel regulator of VSMC proliferation that represses neointimal formation by inhibiting LRRFIP1 expression.
2013-04-23 | GSE45433 | 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:Acute vascular injury is an unwelcome consequence of invasive treatments designed to alleviate symptoms of vascular stenosis. Resulting fibrotic scarring and neointima formation may result in loss of lumen diameter and diminished vascular function. Understanding of the key phases of acute inflammation, resolution and remodeling has the potential to minimise unwanted effects on the vasculature and therefore improve patient outcomes. The cellular landscape of blood vessels is highly hetergeneous in nature, and therefore data at single-cell resolution is of high relevance to this problem. Herein, the cellularity of murine carotid artery tissue is described in a cell- and time-resolved manner. Single-cell RNA-sequencing of carotid tissue isolated at time-points ranging from uninjured vessel to 14 days post-injury enabled the recapitulation of all stages of vascular injury. In these data, a sub-population of smooth muscle cells which also arises in atherosclerosis and myocardial infarction was identified. So-called stem cells/endothelial cells/monocytes (SEM) cells are candidates for repopulating injured vessels, and were amongst the most proliferative cell clusters following wire-injury of the carotid artery. Transcriptional signatures reflecting SEM gene expression patterns could also be detected in bulk RNA-sequencing of neointimal tissue isolated by laser capture microdissection. These data indicate that phenotypic plasticity of smooth muscle cells is highly important to the progression of lumen loss following acute vascular insult.
2023-03-09 | GSE217801 | GEO
Project description:Analysis of carotid artery vessels from wild-type and collagen type VIII deletion mice
2021-05-13 | MSV000087422 | MassIVE
Project description:Single-cell transcriptome of the murine carotid artery following acute injury
| PRJNA900576 | ENA
Project description:Acute vascular injury is an unwelcome consequence of invasive treatments designed to alleviate symptoms of vascular stenosis. Resulting fibrotic scarring and neointima formation may result in loss of lumen diameter and diminished vascular function. Understanding of the key phases of acute inflammation, resolution and remodeling has the potential to minimise unwanted effects on the vasculature and therefore improve patient outcomes. The cellular landscape of blood vessels is highly hetergeneous in nature, and therefore data at single-cell resolution is of high relevance to this problem. Herein, the cellularity of murine carotid artery tissue is described in a cell- and time-resolved manner. Single-cell RNA-sequencing of carotid tissue isolated at time-points ranging from uninjured vessel to 14 days post-injury enabled the recapitulation of all stages of vascular injury. In these data, a sub-population of smooth muscle cells which also arises in atherosclerosis and myocardial infarction was identified. So-called stem cells/endothelial cells/monocytes (SEM) cells are candidates for repopulating injured vessels, and were amongst the most proliferative cell clusters following wire-injury of the carotid artery. Transcriptional signatures reflecting SEM gene expression patterns could also be detected in bulk RNA-sequencing of neointimal tissue isolated by laser capture microdissection. These data indicate that phenotypic plasticity of smooth muscle cells is highly important to the progression of lumen loss following acute vascular insult.
2023-03-09 | GSE220779 | GEO
Project description:The whole rat genome microarray expression profiling of carotid artery specimen was emplyed to identify the gene expression profile before and after balloon injury. In our study, the neointimal formation of carotid arteries was apparent at day 7 and markedly increased at day 21 after balloon injury. In order to investigate the underlying mechanism of neointimal formationin in injured carotid arteries, all genes involved in signaling pathways whose expression was altered 2-fold in injured carotid arteries at day 7 and day 21 as compared to uninjured arteries were filtered out. Expression of four genes (TLR4, IRAK1, IM-NM-:BM-NM-1, IL-1M-NM-2) from TLR signaling pathway was quantified in the same RNA samples by quantitative real-time PCR, conforming that TLR signaling pathway participated in neointimal formation of carotid arteries after balloon injury. Balloon injury-induced gene expression in wistar rat was measured at day 7 and day 21 after balloon injury as compared with uninjured arteries. Two independent experiments were performed at each time (uninjured, day 7 or day 21) using different wistar rats for each experiment.
2013-06-29 | E-GEOD-48279 | biostudies-arrayexpress