Similar Datasets
Project description:Whole transcriptome deep sequencing to rat vein graft
| PRJNA627619 | ENA
Project description:Occlusive artery disease (CAD) is the leading cause of death worldwide. Bypass graft surgery remains the prevalently performed treatments for occlusive arterial disease, and veins are the most frequently used conduits for surgical revascularization. However, clinical efficacy is highly affected by the long-term potency rates of vein grafts, and no optimal treatments are available for prevention of vein graft restenosis (VGR) until today. Therefore, it is urgent to improve the understanding of molecular mechanisms involved in mediating VGR, and thereby provide potential potent therapeutic targets for prevention of vein graft failure. In this study, we aim to explore potential crucial genes and pathways associated with VGR and provide valid biological information for further investigation of VGR.
2018-05-23 | GSE110398 | GEO
Project description:PCSK9 promotes vein graft lesion development
| PRJNA862083 | ENA
Project description:To explore a novel mechanism of macrophage activation and vein graft disease induced by circulating PCSK9 in an LDLR-independent fashion
2023-03-30 | GSE209669 | GEO
Project description:Gene expression profiling of vein graft restenosis
| PRJNA433625 | ENA
Project description:To further development of our gene expression approach to cardiovascular disease, we have employed microarray expression profiling as a discovery platform to identify genes with the potential to distinguish the therapeutic target of the vein graft restenosis following coronary artery bypass grafting. Vein graft samples were obtained from model rats which received external jugular vein-carotid bypass grafting at different postoperative timepoints (n=3/group; day 7, 14 and 28, respectively). Vein samples were also obtained from control rats without vascular grafting (n=3/group; day 0). Time-dependent gene expression profiles were described with microarray analysis. Expression of three lncRNA-mRNA pairs (AF062402-Src, BC091437-Edg1 and BC166461- Mcam) from this signature were quantified in the same RNA samples by real-time PCR, confirming the accuracy of the microarray data.
2020-06-16 | GSE152538 | 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.
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.
2024-05-29 | GSE263280 | GEO
Project description:Acute rejection episodes trigger chronic renal allograft vasculopathy. Numerous leukocytes, predominantly monocytes, accumulate in graft blood vessels during reversible acute rejection preceding chronic rejection of rat kidneys. We speculate that they contribute to transplant vasculopathy and set out to characterize them. Allogeneic renal transplantation was performed in the Fischer 344 to Lewis rat strain combination, Lewis isografts served as controls. Leukocytes were harvested by intensive perfusion of graft blood vessels and subjected to flow cytometry, quantitative RT-PCR and genome-wide transcriptional profiling.
2010-09-24 | GSE18266 | GEO
Project description:Development of gene expression signatures for vein graft restenosis following vascular grafting
| PRJNA639605 | ENA