Loss of endothelial cell heterogeneity in arteries after obesogenic diet [scRNA-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA984740 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24952444_1.fastq.gz | Fastqsanger.gz | |||
| SRR24952444_2.fastq.gz | Fastqsanger.gz | |||
| SRR24952445_1.fastq.gz | Fastqsanger.gz | |||
| SRR24952445_2.fastq.gz | Fastqsanger.gz | |||
| SRR24952446_1.fastq.gz | Fastqsanger.gz |
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Project description:Loss of endothelial cell heterogeneity in arteries after obesogenic diet
| PRJNA984738 | ENA
Project description:Loss of endothelial cell heterogeneity in arteries after obesogenic diet [Bulk-seq]
| PRJNA984739 | ENA
Project description:Background: It is well recognized that obesity leads to arterial endothelial dysfunction and cardiovascular disease. However, the progression to endothelial dysfunction is not clear. Endothelial cells (ECs) adapt to the unique needs of their resident tissue and respond to systemic metabolic perturbations. We sought to better understand how obesity affects EC phenotypes in different tissues specifically focusing on mitochondrial gene expression. Methods: We performed bulk RNA sequencing (RNA-seq) and single cell RNA-seq (scRNA-seq) on mesenteric and adipose ECs isolated from normal chow (NC) and high fat diet (HFD) fed mice. Differential gene expression, gene ontology pathway, and transcription factor analyses were performed. We further investigated our hypothesis in humans using published human adipose single nuclei RNA-seq (snRNA-seq) data. Results: Bulk RNA-seq revealed higher mitochondrial gene expression in adipose ECs compared to mesenteric ECs in both NC and HFD mice. We then performed scRNA-seq and categorized EC clusters as arterial, capillary, venous, or lymphatic. HFD decreased the number of differentially expressed genes between mesenteric and adipose ECs in all subtypes, but the largest effect was seen in arterial ECs. Further analysis of arterial ECs revealed genes coding for mitochondrial oxidative phosphorylation proteins were enriched in adipose compared to mesentery under NC conditions. In HFD mice, these genes were decreased in adipose ECs becoming similar to mesenteric ECs. Transcription factor analysis revealed C/EBP and PPAR, both known to regulate lipid handling and metabolism, had high specificity scores in the NC adipose artery ECs. These findings were recapitulated in snRNA-seq data from human adipose. Conclusions: These data suggest mesenteric and adipose arterial ECs metabolize lipids differently and the transcriptional phenotype of these two vascular beds converge in obesity, in part, due to downregulation of PPARand C/EBP in adipose artery ECs. This work lays the foundation for investigating vascular bed specific adaptations to obesity.
2023-06-26 | GSE235191 | GEO
Project description:Background: It is well recognized that obesity leads to arterial endothelial dysfunction and cardiovascular disease. However, the progression to endothelial dysfunction is not clear. Endothelial cells (ECs) adapt to the unique needs of their resident tissue and respond to systemic metabolic perturbations. We sought to better understand how obesity affects EC phenotypes in different tissues specifically focusing on mitochondrial gene expression. Methods: We performed bulk RNA sequencing (RNA-seq) and single cell RNA-seq (scRNA-seq) on mesenteric and adipose ECs isolated from normal chow (NC) and high fat diet (HFD) fed mice. Differential gene expression, gene ontology pathway, and transcription factor analyses were performed. We further investigated our hypothesis in humans using published human adipose single nuclei RNA-seq (snRNA-seq) data. Results: Bulk RNA-seq revealed higher mitochondrial gene expression in adipose ECs compared to mesenteric ECs in both NC and HFD mice. We then performed scRNA-seq and categorized EC clusters as arterial, capillary, venous, or lymphatic. HFD decreased the number of differentially expressed genes between mesenteric and adipose ECs in all subtypes, but the largest effect was seen in arterial ECs. Further analysis of arterial ECs revealed genes coding for mitochondrial oxidative phosphorylation proteins were enriched in adipose compared to mesentery under NC conditions. In HFD mice, these genes were decreased in adipose ECs becoming similar to mesenteric ECs. Transcription factor analysis revealed C/EBP and PPAR, both known to regulate lipid handling and metabolism, had high specificity scores in the NC adipose artery ECs. These findings were recapitulated in snRNA-seq data from human adipose. Conclusions: These data suggest mesenteric and adipose arterial ECs metabolize lipids differently and the transcriptional phenotype of these two vascular beds converge in obesity, in part, due to downregulation of PPARand C/EBP in adipose artery ECs. This work lays the foundation for investigating vascular bed specific adaptations to obesity.
2023-06-26 | GSE235189 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2023-06-24 | GSE235192 | GEO
Project description:Phenotypic heterogeneity among arterial ECs is particularly relevant to atherosclerosis since the disease occurs predominantly in major arteries, which vary in their atherosusceptibility. To explore EC heterogeneity, we used DNA microarrays to compare gene expression profiles of freshly harvested porcine coronary and iliac artery ECs. We demonstrate that in vivo the endothelial transcriptional profile of a coronary artery (the right coronary artery) is intrinsically different from that of a major conduit vessel (the external iliac artery), and that this difference is consistent with former vessel being more prone to atherosclerosis. Keywords: coronary atherosclerosis, endothelial heterogeneity, microarray, gene expression Endothelial cells were freshly harvest from right coronary, left and right iliac arteries from four pigs. RNA were isolated and expression profiles were obtained using olig microarrays.
2010-06-20 | E-GEOD-10938 | biostudies-arrayexpress
Project description:Phenotypic heterogeneity among arterial ECs is particularly relevant to atherosclerosis since the disease occurs predominantly in major arteries, which vary in their atherosusceptibility. To explore EC heterogeneity, we used DNA microarrays to compare gene expression profiles of freshly harvested porcine coronary and iliac artery ECs. We demonstrate that in vivo the endothelial transcriptional profile of a coronary artery (the right coronary artery) is intrinsically different from that of a major conduit vessel (the external iliac artery), and that this difference is consistent with former vessel being more prone to atherosclerosis. Keywords: coronary atherosclerosis, endothelial heterogeneity, microarray, gene expression
2008-08-23 | GSE10938 | GEO
Project description:Fibroblast heterogeneity revealed by single cell sequencing in healthy and atherosclerotic arteries
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Project description:Endothelial cell (EC) metabolism regulates angiogenesis and is an emerging target for anti-angiogenic therapy in tumor and choroidal neovascularization (CNV). In contrast to tumor ECs (TECs), CNV-ECs cannot be isolated for unbiased metabolic target discovery. Here we used scRNA-sequencing to profile 28,337 choroidal ECs (CECs) from mice to in silico distinguish healthy CECs from CNV-ECs. Trajectory inference suggested that CNV-ECs plastically upregulate genes in central carbon metabolism and collagen biosynthesis during differentiation from quiescent postcapillary venous ECs. CEC-tailored genome scale metabolic modeling predicted essentiality of SQLE and ALDH18A1 for proliferation and collagen production, respectively. Comparative analysis in TECs revealed more outspoken metabolic transcriptome heterogeneity in subtypes and consistent upregulation of SQLE and ALDH18A1 across tumor types. Inhibition of SQLE and ALDH18A1 reduced sprouting angiogenesis in vitro. These findings demonstrate the potential of integrated scRNA-seq analysis to identify angiogenic metabolic targets in disease ECs.
2020-06-25 | E-MTAB-8119 | biostudies-arrayexpress
Project description:Endothelial cell (EC) metabolism is an emerging target for anti-angiogenic therapy in tumor and choroidal neovascularization (CNV), but little is known about individual EC metabolic transcrip-tomes. Here, by scRNA-sequencing 28,337 murine choroidal ECs (CECs) and sprouting CNV-ECs, we constructed a taxonomy to characterize their heterogeneity. Comparison with murine lung tumor ECs (TECs) revealed congruent marker gene expression by distinct EC phenotypes across tissues and diseases, suggesting similar angiogenic mechanisms. Trajectory inference of CNV-ECs revealed that differentiation of venous to angiogenic ECs was accompanied by metabolic transcriptome plasticity. EC phenotypes displayed metabolic transcriptome heterogeneity. Hypothesizing that conserved genes are more important, we used an integrated analysis, based on congruent transcriptome analysis, CEC-tailored genome scale metabolic modeling, and gene expression me-ta-analysis in multiple cross-species datasets, followed by functional validation, to identify the top-ranking metabolic targets SQLE and ALDH18A1, involved in EC proliferation and collagen production, respectively, as novel angiogenic targets.
2020-03-31 | E-MTAB-8604 | biostudies-arrayexpress