Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-cell and spatial transcriptomics uncovers the role of senescent vascular cells in pathological arterial remodeling during murine atherosclerosis

ABSTRACT: Single-cell and spatial transcriptomics uncovers the role of senescent vascular cells in pathological arterial remodeling during murine atherosclerosis

PROVIDER: PRJNA999736 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR25454419.fastq.gz	Fastqsanger.gz
	SRR25454420.fastq.gz	Fastqsanger.gz
	SRR25454421.fastq.gz	Fastqsanger.gz
	SRR25454422.fastq.gz	Fastqsanger.gz
	SRR25454423.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Single-cell and spatial transcriptomics uncovers the role of senescent vascular cells in pathological arterial remodeling during murine atherosclerosis

Project description:Single-cell and spatial transcriptomics uncovers the role of senescent vascular cells in pathological arterial remodeling during murine atherosclerosis

| PRJNA999750 | ENA

Single-cell and spatial transcriptomics uncovers the role of senescent vascular cells in pathological arterial remodeling during murine atherosclerosis

Project description:Studying cardiovascular senescence is crucial in understanding the diverse manifestations of disease-related changes in the cardiovascular system and their implications for overall health and disease. To systematically investigate the heterogeneity of senescent vascular cells in atherosclerosis, we employed the senescence reporter mouse p16TdTomato+/-, injected with an adeno-associated virus expressing PCSK9 to induce atherosclerosis when fed a high-fat diet (HFD). We then treated this mouse with the senolytic drug ABT-737 or vehicle. Whole-aorta single-cell RNA-sequencing (scRNA-seq) and Gene Set Enrichment Analysis (GSEA) using the SenMayo panel, uncovered 10 cell clusters displaying increased senescent features that were reduced by treatment with ABT-737. Interestingly, these clusters do not express ‘classical’ senescence markers such as p16 and p21, but were senescent based on SenMayo GSEA, indicating that the senescence transcriptomic signature in this niche requires deeper characterization. Using unbiased subclustering of the top four potentially senescent clusters, we identified subsets of cells increasing by HFD and reduced by ABT-737 treatment. Accordingly, unique transcripts associated with each subpopulation, such as Spp1, Ctsb, and Tnfrsf11b, implicated these cells in senescence-related signaling pathways. We then validated these findings by spatial transcriptomic profiling, locating senescent cells in the cap and core of brachiocephalic arteries from atherosclerotic mice. Our results uncover a new vascular-specific transcriptomic signature that may be exploited for therapeutic targeting in age-related vascular diseases.

2025-03-05 | GSE239591 | GEO

Single-cell and spatial transcriptomics uncovers the role of senescent vascular cells in pathological arterial remodeling during murine atherosclerosis

2024-07-28 | GSE239602 | GEO

Senescent cells suppress innate VSMC repair functions in atherosclerosis

Project description:Senescent cells suppress innate VSMC repair functions in atherosclerosis

| PRJNA702591 | ENA

Intermittent childhood hyperlipidaemia alters resident arterial macrophages and accelerates atherosclerosis

Project description:Intermittent childhood hyperlipidaemia alters resident arterial macrophages and accelerates atherosclerosis

| PRJEB60780 | ENA

Intermittent childhood hyperlipidaemia alters resident arterial macrophages and accelerates atherosclerosis

Project description:Intermittent childhood hyperlipidaemia alters resident arterial macrophages and accelerates atherosclerosis

| PRJEB60746 | ENA

CEBPB drives endothelial pathological phenotype and promotes atherosclerosis by directly upregulating TGFBR1 expression [RNA-seq]

Project description:Endothelial cell (EC) dysfunction is crucial in chronic vascular inflammation and diseases like atherosclerosis. An unknown endothelial pathological phenotype potentially driving atherosclerosis was hinted in our previous study. However, the detailed characterizations and underlying molecular mechanisms remain unclear. In the present study, using single-cell RNA sequencing, the new endothelial pathological phenotype was defined by high expression of fibroblast markers, extracellular matrix, and inflammatory genes, concurrently with a rapid decline in endothelial markers. By performing RNA-seq, we found that increased CEBPB contributes to the fibroblast and inflammatory feature of these atherogenic ECs. Further analysis revealed that IL-1β-induced high expression of CEBPB triggers TGF-β signaling and subsequent regulation of downstream genes. This occurs through direct interaction of CEBPB with the promotor region of TGF-β receptor type I (TGFBR1), resulting in its upregulation. Furthermore, exacerbating atherosclerotic plaque area, enhanced vascular inflammation and increased endothelial TGFBR1 expression were confirmed by endothelial overexpression of CEBPB in vivo. These findings suggest endothelial CEBPB functions as a novel regulator of TGFBR1, driving endothelial pathological phenotype, promoting vascular inflammation and atherosclerosis.

2025-12-10 | GSE278347 | GEO

CEBPB drives endothelial pathological phenotype and promotes atherosclerosis by directly upregulating TGFBR1 expression [CUT&Tag-Seq]

Project description:Endothelial cell (EC) dysfunction is crucial in chronic vascular inflammation and diseases like atherosclerosis. An unknown endothelial pathological phenotype potentially driving atherosclerosis was hinted in our previous study. However, the detailed characterizations and underlying molecular mechanisms remain unclear. In the present study, using single-cell RNA sequencing, the new endothelial pathological phenotype was defined by high expression of fibroblast markers, extracellular matrix, and inflammatory genes, concurrently with a rapid decline in endothelial markers. Further analysis revealed that increased CEBPB contributes to the fibroblast and inflammatory feature of these atherogenic ECs, which was further confirmed in cultured human aortic ECs. Mechanistically, IL-1β-induced high expression of CEBPB triggers TGF-β signaling and subsequent regulation of downstream genes. By performing CUT&Tag analysis, we further investigated that CEBPB directly regulates TGFBR1 expression in endothelial cells through direct interaction of CEBPB with the promotor region of TGF-β receptor type I (TGFBR1). These findings suggest endothelial CEBPB functions as a novel regulator of TGFBR1, driving endothelial pathological phenotype, promoting vascular inflammation and atherosclerosis.

2025-12-10 | GSE278348 | GEO

CEBPB drives endothelial pathological phenotype and promotes atherosclerosis by directly upregulating TGFBR1 expression [scRNA-seq]

Project description:Endothelial cell (EC) dysfunction is crucial in chronic vascular inflammation and diseases like atherosclerosis. An unknown endothelial pathological phenotype potentially driving atherosclerosis was hinted in our previous study. However, the detailed characterizations and underlying molecular mechanisms remain unclear. Here, we have defined a new endothelial pathological phenotype, characterized by high expression of fibroblast and pro-inflammatory genes with a rapid reduction in EC fate genes by performing single-cell RNA sequencing. Further analysis revealed that increased CEBPB contributes to the fibroblast and inflammatory feature of these atherogenic ECs, which was further confirmed in cultured human aortic ECs. Mechanistically, IL-1β-induced high expression of CEBPB triggers TGF-β signaling and subsequent regulation of downstream genes. This occurs through direct interaction of CEBPB with the promotor region of TGF-β receptor type I (TGFBR1), resulting in its upregulation. Furthermore, exacerbating atherosclerotic plaque area, enhanced vascular inflammation and increased endothelial TGFBR1 expression were confirmed by endothelial overexpression of CEBPB in vivo. These findings suggest endothelial CEBPB functions as a novel regulator of TGFBR1, driving endothelial pathological phenotype, promoting vascular inflammation and atherosclerosis. Targeting endothelial CEBPB may offer new therapeutic avenues for atherosclerotic diseases.

2025-12-10 | GSE278346 | GEO

Smooth muscle cell-specific translatome profiling of mouse atherosclerosis uncovers Itih4 as a novel SMC-enriched gene

Project description:The development of atherosclerosis, a chronic disease characterized by the buildup of plaque in arterial walls, involves the contribution of vascular smooth muscle cells (SMCs) and SMC-derived cells. To better understand the specific role of SMCs in atherosclerosis, a transgenic mouse line expressing EGFP-tagged ribosomal protein L10a (EGFP-L10a) under the SMC-specific αSMA promoter (SMCTRAP mice) was developed, enabling translating ribosome affinity purification followed by sequencing (TRAP-Seq). SMCTRAP mice were crossed with an atherosclerosis model (SMCTRAP-Athero mice). Using TRAP-Seq and bulk RNA-Seq, the aortas of 15-month-old SMCTRAP and SMCTRAP-Athero mice were analyzed to identify atherosclerosis-induced changes in the profiles of SMC ribosome-associated RNA. The results showed high enrichment of known SMC-specific genes in the TRAP fraction, indicating the specificity of the construct. The intersection of SMC-specific genes identified by TRAP-Seq, and atherosclerosis-induced genes identified by bulk RNA-Seq revealed the contribution of SMCs to the expression of several known disease-induced genes, as well as the identification of previously unlinked genes in atherosclerosis that warrant further investigation. These findings provide new insights into the role of SMCs in atherosclerosis and may offer potential targets for future treatments of this chronic disease.

2024-02-08 | GSE225424 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data