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Histone deacetylase inhibition enhances self renewal and cardioprotection by human cord blood-derived CD34 cells.
- Source :
-
PloS one [PLoS One] 2011; Vol. 6 (7), pp. e22158. Date of Electronic Publication: 2011 Jul 18. - Publication Year :
- 2011
-
Abstract
- Background: Use of peripheral blood- or bone marrow-derived progenitors for ischemic heart repair is a feasible option to induce neo-vascularization in ischemic tissues. These cells, named Endothelial Progenitors Cells (EPCs), have been extensively characterized phenotypically and functionally. The clinical efficacy of cardiac repair by EPCs cells remains, however, limited, due to cell autonomous defects as a consequence of risk factors. The devise of "enhancement" strategies has been therefore sought to improve repair ability of these cells and increase the clinical benefit.<br />Principal Findings: Pharmacologic inhibition of histone deacetylases (HDACs) is known to enhance hematopoietic stem cells engraftment by improvement of self renewal and inhibition of differentiation in the presence of mitogenic stimuli in vitro. In the present study cord blood-derived CD34(+) were pre-conditioned with the HDAC inhibitor Valproic Acid. This treatment affected stem cell growth and gene expression, and improved ischemic myocardium protection in an immunodeficient mouse model of myocardial infarction.<br />Conclusions: Our results show that HDAC blockade leads to phenotype changes in CD34(+) cells with enhanced self renewal and cardioprotection.
- Subjects :
- Acetylation drug effects
Animals
Biomarkers metabolism
Cell Proliferation drug effects
Clone Cells
Cluster Analysis
Flow Cytometry
Gene Expression Profiling
Humans
Mice
Phenotype
Regeneration drug effects
Stem Cells cytology
Stem Cells metabolism
Valproic Acid pharmacology
Wound Healing drug effects
Antigens, CD34 metabolism
Cardiotonic Agents pharmacology
Fetal Blood cytology
Histone Deacetylase Inhibitors pharmacology
Histone Deacetylases metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1932-6203
- Volume :
- 6
- Issue :
- 7
- Database :
- MEDLINE
- Journal :
- PloS one
- Publication Type :
- Academic Journal
- Accession number :
- 21789227
- Full Text :
- https://doi.org/10.1371/journal.pone.0022158