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Text
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<a href="http://doi.org/10.1161/circulationaha.111.082453" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/circulationaha.111.082453</a>
Pages
314–324
Issue
3
Volume
126
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Title
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Myocardial CXCR4 expression is required for mesenchymal stem cell mediated repair following acute myocardial infarction.
Publisher
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Circulation
Date
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2012
2012-07-17
Subject
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Mice; Myocardium; Cells; Receptors; Proteins; Animal Studies; Cell Physiology; Cardiovascular System Physiology; Myocardial Infarction; Myocardial Infarction – Therapy; Stem Cells – Metabolism; Cytokines – Metabolism; Cell Surface – Metabolism; Myocardial Infarction – Pathology; Apoptosis – Physiology; Cell Movement – Physiology; Cell Surface; Coronary Circulation – Physiology; Gene Expression – Physiology; Stem Cells – Transplantation
Creator
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Dong F; Harvey J; Finan A; Weber K; Agarwal U; Penn M S
Description
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BACKGROUND: Overexpression of stromal cell-derived factor-1 in injured tissue leads to improved end-organ function. In this study, we quantify the local trophic effects of mesenchymal stem cell (MSC) stromal cell-derived factor-1 release on the effects of MSC engraftment in the myocardium after acute myocardial infarction. METHODS AND RESULTS: Conditional cardiac myocyte CXCR4 (CM-CXCR4) null mice were generated by use of tamoxifen-inducible cardiac-specific cre by crossing CXCR4 floxed with MCM-cre mouse. Studies were performed in littermates with (CM-CXCR4 null) or without (control) tamoxifen injection 3 weeks before acute myocardial infarction. One day after acute myocardial infarction, mice received 100 000 MSC or saline via tail vein. We show [alpha]-myosin heavy chain MerCreMer and the MLC-2v promoters are active in cardiac progenitor cells. MSC engraftment in wild-type mice decreased terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling positive CM (-44%, P\textless0.01), increased cardiac progenitor cell recruitment (100.9%, P\textless0.01), and increased cardiac myosin-positive area (39%, P\textless0.05) at 4, 7, and 21 days after acute myocardial infarction, respectively. MSC in wild-type mice resulted in 107.4% (P\textless0.05) increase in ejection fraction in comparison with 25.9% (P=NS) increase in CM-CXCR4 null mice. These differences occurred despite equivalent increases (16%) in vascular density in response to MSC infusion in wild-type and CM-CXCR4 null mice. CONCLUSIONS: These data demonstrate that the local trophic effects of MSC require cardiac progenitor cell and CM-CXCR4 expression and are mediated by MSC stromal cell-derived factor-1 secretion. Our results further demonstrate and quantify for the first time a specific paracrine mechanism of MSC engraftment. In the absence of CM-CXCR4 expression, there is a significant loss of functional benefit in MSC-mediated repair despite equal increases in vascular density.
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<a href="http://doi.org/10.1161/circulationaha.111.082453" target="_blank" rel="noreferrer noopener">10.1161/circulationaha.111.082453</a>
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2012
Agarwal U
Animal Studies
Apoptosis – Physiology
Cardiovascular System Physiology
Cell Movement – Physiology
Cell Physiology
Cell Surface
Cell Surface – Metabolism
Cells
Circulation
Coronary Circulation – Physiology
Cytokines – Metabolism
Department of Integrative Medical Sciences
Dong F
Finan A
Gene Expression – Physiology
Harvey J
Mice
myocardial infarction
Myocardial Infarction – Pathology
Myocardial Infarction – Therapy
Myocardium
NEOMED College of Medicine
Penn M S
Proteins
Receptors
Stem Cells – Metabolism
Stem Cells – Transplantation
Weber K