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Single cell RNA sequencing of distal thrombus tissue from CTEPH patients

ABSTRACT: Single cell RNA sequencing of distal thrombus tissue from CTEPH patients

PROVIDER: PRJNA929967 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23290213_1.fastq.gz	Fastqsanger.gz
	SRR23290213_2.fastq.gz	Fastqsanger.gz
	SRR23290214_1.fastq.gz	Fastqsanger.gz
	SRR23290214_2.fastq.gz	Fastqsanger.gz
	SRR23290215_1.fastq.gz	Fastqsanger.gz

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Single cell RNA sequencing of distal thrombus tissue from CTEPH patients

Project description:Our current understanding of CTEPH pathobiology is primarily derived from cell-based studies limited by the use of specific cell markers or phenotypic modulation in cell culture. Therefore, our main objective is to identify the multiple cell types that comprise the CTEPH thrombus and to study their dysfunction. Here we used single cell RNA sequencing (scRNAseq) of tissue removed at the time of pulmonary endarterectomy (PEA) surgery from five patients to identify the multiple cell types. Our scRNAseq identify the multiple cell types including macrophages, T cells, and smooth muscle cells, that comprise CTEPH thrombus. Notably, multiple macrophage subclusters were identified but broadly split into two categories, with the larger group characterized by an upregulation of inflammatory signaling predicted to promote pulmonary vascular remodeling. Both CD4+ and CD8+ T cells were identified and likely contribute to chronic inflammation in CTEPH. Smooth muscle cells were a heterogeneous population, with a cluster of myofibroblasts that express markers of fibrosis and are predicted to arise from other smooth muscle cell clusters based on pseudotime analysis. Lastly, our analysis identified protease-activated receptor 1 (PAR1) as a potential therapeutic target that links thrombosis to chronic PE in CTEPH

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Disturbed flow in the juxta-anastomotic area of an arteriovenous fistula correlates with endothelial loss, acute thrombus formation and neointimal hyperplasia

Project description:Background: Clinical failure of arteriovenous fistulae (AVF) is frequently due to juxta-anastomotic neointimal hyperplasia (JANIH). Although the mouse AVF model recapitulates human AVF maturation, previous studies focused on the outflow vein distal to the anastomosis. We hypothesized that the juxta-anastomotic area (JAA) has increased NIH compared to the outflow vein. Method: AVF were created in C57BL/6 mice without or with chronic kidney disease (CKD). Temporal and spatial changes of the JAA were examined using histology and immunofluorescence. Computational techniques were used to model the AVF. RNA-seq and bioinformatic analyses were performed to compare the JAA with the outflow vein. The jugular vein to carotid artery AVF model was created in Wistar rats. Result: The neointima in the JAA shows increased volume compared to the outflow vein. Computational modeling shows increased volume of disturbed flow at the JAA compared to the outflow vein. Endothelial cells are immediately lost from the wall contralateral to the fistula exit, followed by thrombus formation and JANIH. Gene Ontology (GO) enrichment analysis of the 1862 differentially expressed genes (DEG) between the JANIH and the outflow vein identified 525 overexpressed genes. The rat jugular vein to carotid artery AVF showed changes similar to the mouse AVF. Conclusion: Disturbed flow through the JAA correlates with rapid endothelial cell loss, thrombus formation, and JANIH; late endothelialization of the JAA channel correlates with late AVF patency. Early thrombus formation in the JAA may influence later development of JANIH.

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