Document Detail

Myocardial regeneration by transplantation of modified endothelial progenitor cells expressing SDF-1 in a rat model.
MedLine Citation:
PMID:  22288686     Owner:  NLM     Status:  MEDLINE    
Cell based therapy has been shown to attenuate myocardial dysfunction after myocardial infarction (MI) in different acute and chronic animal models. It has been further shown that stromal-cell derived factor-1α (SDF-1α) facilitates proliferation and migration of endogenous progenitor cells into injured tissue. The aim of the present study was to investigate the role of exogenously applied and endogenously mobilized cells in a regenerative strategy for MI therapy. Lentivirally SDF-1α-infected endothelial progenitor cells (EPCs) were injected after 90 min. of ligation and reperfusion of the left anterior descending artery (LAD) intramyocardial and intracoronary using a new rodent catheter system. Eight weeks after transplantation, echocardiography and isolated heart studies revealed a significant improvement of LV function after intramyocardial application of lentiviral with SDF-1 infected EPCs compared to medium control. Intracoronary application of cells did not lead to significant differences compared to medium injected control hearts. Histology showed a significantly elevated rate of apoptotic cells and augmented proliferation after transplantation of EPCs and EPCs + SDF-1α in infarcted myocardium. In addition, a significant increased density of CD31(+) vessel structures, a lower collagen content and higher numbers of inflammatory cells after transplantation of SDF-1 transgenic cells were detectable. Intramyocardial application of lentiviral-infected EPCs is associated with a significant improvement of myocardial function after infarction, in contrast to an intracoronary application. Histological results revealed a significant augmentation of neovascularization, lower collagen content, higher numbers of inflammatory cells and remarkable alterations of apoptotic/proliferative processes in infarcted areas after cell transplantation.
Alexander Schuh; Andreas Kroh; Simone Konschalla; Elisa A Liehn; Radoslav M Sobota; Erik Al Biessen; Ilze Bot; Tolga Taha Sönmez; Sönmez Tolga Taha; Andreas Schober; Nikolaus Marx; Christian Weber; Alexander Sasse
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cellular and molecular medicine     Volume:  16     ISSN:  1582-4934     ISO Abbreviation:  J. Cell. Mol. Med.     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-09-27     Completed Date:  2013-03-26     Revised Date:  2014-02-10    
Medline Journal Info:
Nlm Unique ID:  101083777     Medline TA:  J Cell Mol Med     Country:  England    
Other Details:
Languages:  eng     Pagination:  2311-20     Citation Subset:  IM    
Copyright Information:
© 2012 The Authors Journal of Cellular and Molecular Medicine © 2012 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.
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MeSH Terms
Cardiac Catheterization / methods
Cell Proliferation
Chemokine CXCL12 / genetics*,  metabolism
Collagen / metabolism
Endothelial Cells / metabolism,  transplantation*
Gene Expression Regulation
HEK293 Cells
In Situ Nick-End Labeling
Inflammation / pathology
Models, Animal
Myocardial Infarction / pathology,  therapy
Myocardium / metabolism*
Neovascularization, Pathologic / pathology,  therapy
Rats, Sprague-Dawley
Spleen / cytology,  metabolism
Stem Cell Transplantation
Stem Cells / metabolism*
Reg. No./Substance:
0/CXCL12 protein, rat; 0/Chemokine CXCL12; 9007-34-5/Collagen
Erratum In:
J Cell Mol Med. 2013 Nov;17(11):1513
Note: Tolga Taha, Sönmez [corrected to Sönmez, Tolga Taha]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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