Document Detail


VEGF/SDF-1 promotes cardiac stem cell mobilization and myocardial repair in the infarcted heart.
MedLine Citation:
PMID:  21345805     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
AIMS: The objective of this study was to investigate whether vascular endothelial growth factor (VEGF) secreted by mesenchymal stem cells (MSC) improves myocardial survival and the engraftment of implanted MSC in infarcted hearts and promotes recruitment of stem cells through paracrine release of myocardial stromal cell-derived factor-1α (SDF-1α).
METHODS AND RESULTS: VEGF-expressing MSC ((VEGF)MSC)-conditioned medium enhanced SDF-1α expression in heart slices and H9C2 cardiomyoblast cells via VEGF and the vascular endothelial growth factor receptor (VEGFR). The (VEGF)MSC-conditioned medium markedly promoted cardiac stem cell (CSC) migration at least in part via the SDF-1α/CXCR4 pathway and involved binding to VEGFR-1 and VEGFR-3. In vivo, (VEGF)MSC-stimulated SDF-1α expression in infarcted hearts resulted in massive mobilization and homing of bone marrow stem cells and CSC. Moreover, VEGF-induced SDF-1α guided the exogenously introduced CSC in the atrioventricular groove to migrate to the infarcted area, leading to a reduction in infarct size. Functional studies showed that (VEGF)MSC transplantation stimulated extensive angiomyogenesis in infarcted hearts as indicated by the expression of cardiac troponin T, CD31, and von Willebrand factor and improved the left ventricular performance, whereas blockade of SDF-1α or its receptor by RNAi or antagonist significantly diminished the beneficial effects of (VEGF)MSC.
CONCLUSION: Exogenously expressed VEGF promotes myocardial repair at least in part through SDF-1α/CXCR4-mediated recruitment of CSC.
Authors:
Jun-Ming Tang; Jia-Ning Wang; Lei Zhang; Fei Zheng; Jian-Ye Yang; Xia Kong; Lin-Yun Guo; Long Chen; Yong-Zhang Huang; Yu Wan; Shi-You Chen
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-02-22
Journal Detail:
Title:  Cardiovascular research     Volume:  91     ISSN:  1755-3245     ISO Abbreviation:  Cardiovasc. Res.     Publication Date:  2011 Aug 
Date Detail:
Created Date:  2011-07-20     Completed Date:  2011-11-23     Revised Date:  2014-09-19    
Medline Journal Info:
Nlm Unique ID:  0077427     Medline TA:  Cardiovasc Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  402-11     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Antigens, CD31 / metabolism
Cell Movement*
Cells, Cultured
Chemokine CXCL12 / genetics,  metabolism*
Culture Media, Conditioned / metabolism
Disease Models, Animal
Humans
Mesenchymal Stem Cell Transplantation*
Mesenchymal Stromal Cells / metabolism*
Muscle Development
Myocardial Infarction / metabolism,  pathology,  physiopathology,  surgery*
Myocytes, Cardiac / metabolism*,  pathology
Neovascularization, Physiologic
Paracrine Communication
RNA Interference
Rats
Rats, Sprague-Dawley
Receptors, CXCR4 / metabolism
Recovery of Function
Regeneration*
Time Factors
Transfection
Troponin T / metabolism
Vascular Endothelial Growth Factor A / genetics,  metabolism*
Vascular Endothelial Growth Factor Receptor-1 / metabolism
Vascular Endothelial Growth Factor Receptor-3 / metabolism
Ventricular Function, Left
von Willebrand Factor / metabolism
Grant Support
ID/Acronym/Agency:
HL093429/HL/NHLBI NIH HHS; R01 HL093429/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Antigens, CD31; 0/Chemokine CXCL12; 0/Culture Media, Conditioned; 0/Cxcr4 protein, rat; 0/Receptors, CXCR4; 0/Troponin T; 0/VEGFA protein, human; 0/Vascular Endothelial Growth Factor A; 0/von Willebrand Factor; EC 2.7.10.1/Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1/Vascular Endothelial Growth Factor Receptor-3
Comments/Corrections
Comment In:
Cardiovasc Res. 2011 Aug 1;91(3):369-70   [PMID:  21705348 ]

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