MRNA-seq of bypass grafts in mice, utilizing the vena cava as carotid artery bypass graft
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA489494 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7790280.fastq.gz | Fastqsanger.gz | |||
| SRR7790281.fastq.gz | Fastqsanger.gz | |||
| SRR7790272.fastq.gz | Fastqsanger.gz | |||
| SRR7790282.fastq.gz | Fastqsanger.gz | |||
| SRR7790273.fastq.gz | Fastqsanger.gz |
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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:Single-cell RNA-sequencing of carotid artery ,vein graft and vena cava in mouse models
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Project description:Albeit vascular prostheses for the replacement of large arteries (e.g. aorta) are commercially available for decades, small-diameter vascular grafts (e.g., for coronary artery bypass graft surgery) still remain an unmet clinical need. Biostable polymers commonly used for the fabrication of aortic prostheses (e.g., poly(ethylene terephthalate) or expanded poly(tetrafluoroethylene)) have insufficient haemocompatibility to withstand thrombosis at low blood flow characteristic of small arteries (e.g., coronary artery). Hence, researchers endeavor to develop a biodegradable, tissue-engineered vascular graft (TEVG) to avoid the use of autologous blood vessels, such as saphenous vein or internal mammary artery, as conduits during the bypass surgery. Although a number of promising prototypes have been designed to date, none of them passed the pre-clinical trials successfully. Implantation into the ovine or porcine arteries is associated with thrombosis, neointimal hyperplasia, and aneurysms within one-year postoperation, precluding further clinical translation of TEVGs. Among the reasons of such impediment is that pathophysiology of TEVG implantation remains unclear and the molecular events occurring in the TEVG upon its implantation have not been properly investigated hitherto. Here, we for the first time performed a proteomic profiling of the TEVGs (n = 12) implanted into the ovine carotid arteries for one year and suffered from thrombosis to identify the signatures of TEVG failure in an unbiased manner. Contralateral intact ovine carotid arteries (n = 12) have been selected as a control group.
2022-11-26 | PXD036520 | Pride
Project description:While blood vessels have muscular walls that undergo tonic contractions to alter vascular resistance and, thus, control blood flow, lymphatics at the level of the collecting vessels and higher have muscular walls capable of rapid phasic contractions that generate lymph flow in addition to tonic contractions that regulate lymph flow resistance. While the ability of lymphatics to undergo rapid phasic contractions has been known for several centuries, the biological elements governing this phenomenon remain unknown. In an attempt to gain insight into the structural and regulatory elements that give lymphatic vessels their unique contractile capabilities, we utilized two-color microarray analysis to compare the thoracic duct of the rat to the vena cava of the same donor animal. Total cellular RNA was isolated immediately following vessel isolation and amplified in the presence of amino allyl dUTP. The resulting modified aRNA was conjugated to either Cy3 or Cy5 dye prior to hybridization to a rat 5.7K oligonucleotide array. Analysis and filtering of the data obtained from the microarray image yielded several contractile and regulatory genes with altered expression in the thoracic duct relative to the vena cava. Further evaluation of the data obtained in this study may aid in illustrating the unique properties of the lymphatic vessel and its muscular wall. Keywords: Thoracic duct, lymphatics, microarray Four unique thoracic duct/vena cava sample pairs were individually analyzed via two-color microarray analysis yielding 4 biological replicates. To minimize dye bias, a dye balance design was utilized in which the orientation of dye assignment was alternated between vessel pairs (i.e. two thoracic duct samples were labeled with Cy3 and two were labeled with Cy5). Prior to analysis, the data from 2 of the replicates was transformed to accomodate the dye balance such that all thoracic duct data is interpreted as Cy5 and all vena cava data is interpreted as Cy3.
2010-05-15 | E-GEOD-7221 | biostudies-arrayexpress
Project description:Vein graft failure (VGF) following cardiovascular bypass surgery results in significant patient morbidity and cost to the healthcare system. Vein graft injury can occur during autogenous vein harvest and preparation, as well as after implantation into the arterial system, leading to the development of intimal hyperplasia, vein graft stenosis, and, ultimately, bypass graft failure. While previous studies have identified maladaptive pathways that occur shortly after implantation, the specific signaling pathways that occur during vein graft preparation are not well defined and may result in a cumulative impact on VGF. We, therefore, aimed to elucidate the response of the vein conduit wall during harvest and following implantation, probing the key maladaptive pathways driving graft failure with the overarching goal of identifying therapeutic targets for biologic intervention to minimize these natural responses to surgical vein graft injury. Employing a novel approach to investigating vascular pathologies, we harnessed both single-nuclei RNA-sequencing (snRNA-seq) and spatial transcriptomics (ST) analyses to profile the genomic effects of vein grafts after harvest and distension, then compared these findings to vein grafts obtained 24 hours after carotid-cartoid vein bypass implantation in a canine model (n=4). Collectively, we find that vein conduit harvest and distension elicit a prompt genomic response facilitated by distinct cellular subpopulations heterogeneously distributed throughout the vein wall. This response was found to be further exacerbated following vein graft implantation, resulting in a cascade of maladaptive gene regulatory networks. Together, these results suggest that distension initiates the upregulation of pathological pathways that may ultimately contribute to bypass graft failure and presents potential early targets warranting investigation for targeted therapies.
2024-05-29 | GSE263281 | GEO
Project description:Vein graft failure (VGF) following cardiovascular bypass surgery results in significant patient morbidity and cost to the healthcare system. Vein graft injury can occur during autogenous vein harvest and preparation, as well as after implantation into the arterial system, leading to the development of intimal hyperplasia, vein graft stenosis, and, ultimately, bypass graft failure. While previous studies have identified maladaptive pathways that occur shortly after implantation, the specific signaling pathways that occur during vein graft preparation are not well defined and may result in a cumulative impact on VGF. We, therefore, aimed to elucidate the response of the vein conduit wall during harvest and following implantation, probing the key maladaptive pathways driving graft failure with the overarching goal of identifying therapeutic targets for biologic intervention to minimize these natural responses to surgical vein graft injury. Employing a novel approach to investigating vascular pathologies, we harnessed both single-nuclei RNA-sequencing (snRNA-seq) and spatial transcriptomics (ST) analyses to profile the genomic effects of vein grafts after harvest and distension, then compared these findings to vein grafts obtained 24 hours after carotid-cartoid vein bypass implantation in a canine model (n=4). Collectively, we find that vein conduit harvest and distension elicit a prompt genomic response facilitated by distinct cellular subpopulations heterogeneously distributed throughout the vein wall. This response was found to be further exacerbated following vein graft implantation, resulting in a cascade of maladaptive gene regulatory networks. Together, these results suggest that distension initiates the upregulation of pathological pathways that may ultimately contribute to bypass graft failure and presents potential early targets warranting investigation for targeted therapies.
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Project description:ATAC-seq on human posterior vena cava For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
2021-03-30 | GSE170616 | GEO
Project description:ATAC-seq on human posterior vena cava For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
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Project description:ATAC-seq on human posterior vena cava For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
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