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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE44444 | GEO | 2014/05/06

SECONDARY ACCESSION(S): PRJNA190045

REPOSITORIES: GEO

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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

Genomic binding profile of TAL1 in human Endothelial Colony-Forming Cells

2014-05-06 | E-GEOD-44442 | biostudies-arrayexpress

Genomic binding profile of TAL1 in human Endothelial Colony-Forming Cells

2014-05-06 | GSE44442 | GEO

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

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 umbilical cord blood-derived endothelial colony forming cells under serum-free conditions

Project description:Derivation and expansion of human umbilical cord blood-derived endothelial colony forming cells under serum-free conditions - a transcriptome analysis. Endothelial colony forming cells (ECFCs) were isolated from term umbilical cord blood units. ECFCs were expanded under standard, fetal bovine serum (FBS) containing endothelial medium, or transferred to chemically defined endothelial media without FBS. Microarray expression profiling was applied to compare the transcriptome profiles in FBS-containing versus FBS-free culture. Comparison of the expression patterns of ECFCs that were either cultured in FBS-containing medium or in serum-free medium (five replicates each).

2010-07-29 | E-GEOD-20504 | biostudies-arrayexpress

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

Human umbilical cord blood-derived endothelial colony forming cells under serum-free conditions

2010-06-29 | GSE20504 | GEO

Prospective surface marker-based isolation and expansion of fetal endothelial colony-forming cells from human term placenta.

Project description:The term placenta is a highly vascularized tissue and is usually discarded upon birth. Our objective was to isolate clinically relevant quantities of fetal endothelial colony-forming cells (ECFCs) from human term placenta and to compare them to the well-established donor-matched umbilical cord blood (UCB)-derived ECFCs. A sorting strategy was devised to enrich for CD45-CD34+CD31Lo cells prior to primary plating to obtain pure placental ECFCs (PL-ECFCs) upon culture. UCB-ECFCs were derived using a well-described assay. PL-ECFCs were fetal in origin and expressed the same cell surface markers as UCB-ECFCs. Most importantly, a single term placenta could yield as many ECFCs as 27 UCB donors. PL-ECFCs and UCB-ECFCs had similar in vitro and in vivo vessel forming capacities and restored mouse hind limb ischemia in similar proportions. Gene expression profiles were only minimally divergent between PL-ECFCs and UCB-ECFCs, probably reflecting a vascular source versus a circulating source. Finally, PL-ECFCs and UCB-ECFCs displayed similar hierarchies between high and low proliferative colonies. We report a robust strategy to isolate ECFCs from human term placentas based on their cell surface expression. This yielded much larger quantities of ECFCs than UCB, but the cells were comparable in immunophenotype, gene expression, and in vivo functional ability. We conclude that PL-ECFCs have significant bio-banking and clinical translatability potential. Data has been integrated into the Stemformatics web resource http://www.stemformatics.org/datasets/view/6306

2015-03-02 | E-MTAB-3277 | biostudies-arrayexpress

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