E-GEOD-53423 - Comparative analysis of TAL1 binding in TSA-treated versus non-treated Endothelial Colony Forming Cells (ECFCs)
Released on 6 May 2014, last updated on 29 May 2014
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.
Alexander Griffith, Alphonse Chu, Carmen G Palii, Marjorie Brand
Trichostatin A Enhances Vascular Repair by Injected Human Endothelial Progenitors through Increasing the Expression of TAL1-Dependent Genes. Palii CG, Vulesevic B, Fraineau S, Pranckeviciene E, Griffith AJ, Chu A, Faralli H, Li Y, McNeill B, Sun J, Perkins TJ, Dilworth FJ, Perez-Iratxeta C, Suuronen EJ, Allan DS, Brand M. , Europe PMC 24792117