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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: PRJNA999750 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25454000_1.fastq.gz	Fastqsanger.gz
	SRR25454000_2.fastq.gz	Fastqsanger.gz
	SRR25454001_1.fastq.gz	Fastqsanger.gz
	SRR25454001_2.fastq.gz	Fastqsanger.gz
	SRR25454002_1.fastq.gz	Fastqsanger.gz

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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

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

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

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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.

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