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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE53423 | GEO | 2014/05/06

SECONDARY ACCESSION(S): PRJNA231952

REPOSITORIES: GEO

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Project description:Critical limb threatening ischemia (CLTI), the most severe manifestation of peripheral artery disease, results from the chronic blockade of peripheral vessels, usually induced by atherosclerosis. CLTI patients suffer from high risk of amputation of the lower extremities and elevated mortality rates, while they have low options for surgical revascularization due to associated comorbidities. Alternatively, cell-based therapeutic strategies represent an effective and safe approach to promote revascularization and reversal of CLTI. However, the variety in cell types and cell combinations, administration routes or doses applied, have limited their success in clinical trials, being necessary to reach a consensus regarding the optimal “cellular-cocktail” for these patients, prior further application into the clinic. To achieve so, it is essential to understand the mechanisms by which these cells exert their regenerative properties. Herein, we have evaluated and compared, for the first time, the regenerative and vasculogenic potential of endothelial colony forming cells (ECFCs) isolated from either adipose-tissue (AT-ECFCs) or umbilical cord blood (CB-ECFCs), in combination with AT-derived MSCs, in a murine model of CLTI. Furthermore, the long-term molecular changes in CLTI and in response to both combinations have been analyzed in a proteomic quantitative approach. Overall, the administration of AT-MSCs with either AT- or CB-ECFCs, promoted a significant recovery of blood flow in CLTI mice 21 days post-ischemia, which appeared associated to an increased number of vessels in AT treated mice or with wider vessels in CB. Besides, they both modulated the inflammatory and necrotic processes, although the CB group presented the slowest ischemic progression along the assay. Furthermore, many of the protein changes identified are representative of the molecular mechanisms involved in ECFCs and MSCs induced revascularization (immune response, vascular repair, muscle regeneration, etc).

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

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