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Human endothelial colony forming cells (ECFCs) require endothelial protein C receptor (EPCR) for cell cycle progression and angiogenic activity

ABSTRACT: Human endothelial colony forming cells (ECFCs) require endothelial protein C receptor (EPCR) for cell cycle progression and angiogenic activity

PROVIDER: PRJNA1191367 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31527465_1.fastq.gz	Fastqsanger.gz
	SRR31527465_2.fastq.gz	Fastqsanger.gz
	SRR31527466_1.fastq.gz	Fastqsanger.gz
	SRR31527466_2.fastq.gz	Fastqsanger.gz
	SRR31527467_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Human endothelial colony forming cells (ECFCs) require endothelial protein C receptor (EPCR) for cell cycle progression and angiogenic activity

Project description:Vascular repair and regeneration are critical for tissue homeostasis. Endothelial colony forming cells (ECFCs) are vessel-resident progenitors with vasoreparative capacity and they offer an important avenue for allogeneic cytotherapy to achieve perfusion of ischemic tissues. Endothelial Protein C Receptor (EPCR) has been proposed as a reliable marker for vascular endothelial stem cells, but its precise role in ECFC biology remains unknown. The current study has investigated the biological relevance of EPCR in ECFC function. Our data shows that over 95% of ECFCs exhibit high EPCR expression. These levels surpassing CD34 and CD157, positions EPCR as a new robust ECFC immunophenotypic marker, alongside established markers CD31 and CD105. Functionally, depleting ECPR expression in ECFCs significantly diminished angiogenic activity, including proliferation, migration and tube formation. This knockdown also altered normal ECFC barrier function. Transcriptomic analysis indicated that knockdown of EPCR led to enrichment of gene signatures for cell cycle, TGF beta, and focal adhesion kinases and cell cycle arrest in G1 was confirmed ECFCs in which EPCR was depleted. Mechanistically, EPCR knockdown led to increased release of TGFB2 and SMAD2/3 activation, coupled with increased p21, decreased pFAK, and increased transgelin. Additionally, we showed that quiescent ECFCs showed significantly lower EPCR expression when compared to proliferating ECFCs. In agreement with this, cell sorting experiments demonstrated that ECFCs with the highest EPCR expression exhibited the highest clonogenic capacity. In summary, our findings highlight that EPCR expression in ECFCs is critical for their angiogenic activity, by modulating processes such as cell cycle progression, barrier function, and endothelial to mesenchymal transition.

2025-05-30 | GSE282963 | GEO

shRNA mediated knock-down of Tal1 in human Endothelial Colony Forming Cells (ECFCs)

Project description:Endothelial colony-forming cells (ECFCs) have been reported as promising cells for regenerative medicine thanks to their angiorepair properties. Transcription factors are primary determinants of the functional capacity of the cells and TAL1 has been shown as a critical regulator of endothelial lineage in both development and adult life. However, only few (three) TAL1 targets have been identified so far in mouse and human endothelial cells. This microarray experiment, where TAL1 expression was knocked-down, was designed to identify TAL1-dependent genes in primary human endothelial stem/progenitor cells. ECFCs were isolated from three independent cord blood samples (n=3, biological replicates) and cultured in complete EGM-2 medium. The knockdown of TAL1 was induced by infection with lentiviruses expressing an anti-TAL1 shRNA. A scrambled shRNA was used as a negative control. Cells were then harvested for RNA extraction. DNA-free total RNA was isolated with RNeasy Mini Kit and hybridized to the Affymetrix Human Gene 1.0 ST gene expression microarray.

2014-05-06 | E-GEOD-44444 | biostudies-arrayexpress

Comparative analysis of TAL1 binding in TSA-treated versus non-treated Endothelial Colony Forming Cells (ECFCs)

Project description:Endothelial progenitors represent one of the most promising cell-based strategies for vascular repair of ischemic tissue damage, including limb ischemia, myocardial infarction and stroke. We have shown that the transcription factor TAL1 regulates a transcription program that drives the migration and adhesion of ECFCs. Furthermore, treatment of ECFCs with the HDAC inhibitor TSA increases the expression of TAL1-dependent genes and promotes the migration, chemotaxis and adhesion of ECFCs. Finally, ex vivo treatment with TSA also improves the vascular repair properties of ECFCs in vivo when these cells are transplanted in a mouse model of hindlimb ischemia. The goal of this experiment was to test whether TSA treatment of ECFCs affect TAL1 genomic binding. TAL1 ChIP-sequencing was performed from ECFCs that have been treated or not TSA. As negative controls, we performed Mock-ChIP-seq from the same samples using normal IgG instead of the TAL1 antibody. Overall, we find that there is no change in TAL1 genomic binding in ECFCs upon TSA treatment.

2014-05-06 | E-GEOD-53423 | biostudies-arrayexpress

Comparative analysis of TAL1 binding in TSA-treated versus non-treated Endothelial Colony Forming Cells (ECFCs)

2014-05-06 | GSE53423 | GEO

RESTORATION OF NOX4 SIGNALLING REVERSES ENDOTHELIAL COLONY-FORMING CELL ANGIOGENIC DYSFUNCTION ASSOCIATED WITH EXPERIMENTAL AND CLINICAL DIABETES

Project description:Progenitor endothelial colony forming cells (ECFCs) are critical for vascular homeostasis and hold therapeutic potential for ischaemic cardiovascular disease (CVD). As angiogenic capacity and efficacy within diseased tissues is particularly impacted in diabetic patients, who show high incidence of ischaemic CVD, targeting of critical ECFC pathways in this setting represents an innovative focus towards enhancing intrinsic vasoreparative function. We previously reported that NADPH oxidase 4 (NOX4)-derived reactive oxygen species promote cord blood-derived ECFC (CB-ECFC) pro-angiogenic response, whilst NOX4 overexpression (OE) enhances revascularisation capacity. Here, we aimed to investigate specific influence of NOX4-dependent signalling on CB-ECFC angiogenic dysfunction observed upon exposure to both experimental and clinical diabetes to define whether NOX4 may represent a viable therapeutic target in this context.

2025-06-03 | GSE296585 | GEO

shRNA mediated knock-down of Tal1 in human Endothelial Colony Forming Cells (ECFCs)

2014-05-06 | GSE44444 | GEO

Distinct phenotype and proteomic signature of peripheral blood-endothelial colony-forming cells of subjects with varied cardiovascular disease risks

Project description:Endothelial progenitor cells (EPCs) are circulating endothelial precursors shown to incorporate into foci of neovascularisation. Herein, we describe phenotypic characteristics of an EPC sub-type called endothelial colony-forming cells (ECFCs). Peripheral blood-isolated ECFCs expressed endothelial and progenitor surface antigens and displayed cobblestone-patterned colonies with clonal proliferative and angiogenic capacities in vitro. ECFCs demonstrated endothelial cell-like shear stress responses including cell alignment and PECAM-1 expression. Proteomic comparison with an endothelial reference population (human umbilical vein endothelial cells) confirmed a similar proteomic profile. Hierarchical clustering revealed two distinct ECFC clusters with differences in cell growth, proliferation and angiogenesis capacities. The cluster with compromised functionality was also associated with elevated blood pressure and impaired lipid profile. Our findings described an endothelial-like phenotype of blood-derived ECFCs with distinctive proteomic signatures based on cellular and clinical characteristics. ECFCs may aid in identifying novel mechanisms associated with cardiovascular disease risk and new targets to enhance angiogenesis.

2022-02-15 | PXD020677 | Pride

Gene expression profile of Endothelial colony-forming cells (ECFCs) isolated from patients with unprovoked venous thromboembolism (uVTE)

Project description:Anlysis of ECFCs isolated from uVTE patients at gene expression level. The hypothesis tested in the present study was that endothelial dysfunction could be involved in uVTE pathogenesis. Results provide important information on endothelial compartement of uVTE patients identifying either significantly up- and down regulated genes.

2018-08-08 | GSE118259 | GEO

Human ECFCs: Cord Blood vs Peripehral Blood ECFCs

Project description:miRNA profiling was carried out using the miRCURY LNA™ microRNA Array (5th gen - hsa, mmu & rno). microRNA profiling of CB and PB-derived ECFCs from 3 independent donors from each cell source. To identify and understand the regulation of endothelial cell functions through comparing miRNA expression profiling of cord blood (CB) derived endothelial colony forming cells (ECFCs) and peripheral blood (PB) ECFCs

2017-03-20 | GSE81574 | GEO

Genome-wide analysis of gene expression in endothelial colony forming cells and mature endothelial cells

Project description:Autologous endothelial cells are promising alternative angiogenic cell sources in trials of therapeutic vasculogenesis; in the treatment of vascular diseases and in the field of tissue engineering. A population of endothelial cells (ECs) with long-term proliferative capability can be isolated from human peripheral blood. They are called endothelial colony forming cells (ECFCs), and are considered to be an endothelial precursor population. They can be expanded in cell factories to sufficient numbers for clinical applications, but as the number of isolated primary ECs is low, the culture period required may be quite long. Another EC population that is easily available in the autologous setting and may be expanded in vitro through several population doublings are the ECs from adipose tissue (AT-ECs). Through extensive comparisons using whole-genome microarray analysis, morphology, phenotype and functional assays, we wanted to evaluate the potential of these EC populations for use in clinical neovascularization. Global gene expression profiling of ECFCs, AT-ECs and the classical EC population, human umbilical vein ECs showed that the EC populations clustered as unique populations, but very close to each other. By cell surface phenotype and vasculogenic potential in vitro and in vivo we also found the ECFCs to be extremely similar to AT-ECs. These properties, and easy access in the autologous setting, suggest that both AT-ECs and ECFCs may be useful in trials of therapeutic neovascularization. However, AT-ECs may be a more practical alternative for obtaining large quantities of autologous ECs.

2015-09-30 | GSE55695 | GEO

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