Document Detail


Platelet microparticles enhance the vasoregenerative potential of angiogenic early outgrowth cells after vascular injury.
MedLine Citation:
PMID:  20644015     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Angiogenic early outgrowth cells (EOCs) have been reported to contribute to endothelial regeneration and to limit neointima formation after vascular injury. Vascular pathologies comprise platelet activation and concomitant generation of platelet microparticles (PMPs). We hypothesized that PMPs may interact with EOCs in the context of vascular injury and modulate their regenerative potential. METHODS AND RESULTS: Using flow cytometry, confocal microscopy, and scanning electron microscopy, we demonstrated the binding of thrombin/collagen-induced PMPs to EOCs with subsequent membrane assimilation and incorporation. This interaction promoted phenotypic alterations of EOCs with increased expression of endothelial cell markers and transfer of the chemokine receptor CXCR4 to EOCs with enhanced responsiveness to its ligand CXCL12/SDF-1alpha. In addition, PMPs augmented the adhesion of EOCs to extracellular matrix components and to the injured vessel wall and accelerated cytoskeletal reorganization and migration of EOCs. PMPs induced changes in the EOC secretome toward a more proangiogenic profile and amplified the EOC-mediated induction of proliferation, migration, and capillary tube formation by mature endothelial cells. Compared with untreated EOCs, the injection of PMP-treated EOCs resulted in accelerated reendothelialization after arterial denudation injury in athymic nude mice, whereas the EOC-mediated reduction of neointima formation remained unchanged. CONCLUSIONS: Our data provide evidence that PMPs can boost the potential of EOCs to restore endothelial integrity after vascular injury. Major mechanisms involve the enhancement of EOC recruitment, migration, differentiation, and release of proangiogenic factors.
Authors:
Sebastian F Mause; Elisabeth Ritzel; Elisa A Liehn; Mihail Hristov; Kiril Bidzhekov; Gerhard Müller-Newen; Oliver Soehnlein; Christian Weber
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-07-19
Journal Detail:
Title:  Circulation     Volume:  122     ISSN:  1524-4539     ISO Abbreviation:  Circulation     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-08-03     Completed Date:  2010-09-08     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  United States    
Other Details:
Languages:  eng     Pagination:  495-506     Citation Subset:  AIM; IM    
Affiliation:
Medical Faculty, Institute for Molecular Cardiovascular Research, RWTH Aachen University, Aachen, Germany.
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MeSH Terms
Descriptor/Qualifier:
Animals
Biological Markers / metabolism
Blood Platelets / cytology,  physiology*
Carotid Arteries / pathology,  physiology
Carotid Artery Injuries / pathology,  physiopathology*
Cell Communication / physiology
Cell Differentiation / physiology
Cell Division / physiology
Cell Movement / physiology
Cell-Derived Microparticles / physiology*
Cells, Cultured
Chemokine CXCL12 / metabolism
Cytoskeleton / physiology
Disease Models, Animal
Endothelial Cells / cytology,  physiology*
Flow Cytometry
Humans
Mice
Mice, Inbred C57BL
Mice, Nude
Neovascularization, Physiologic / physiology*
Receptors, CXCR4 / metabolism
Regeneration / physiology
Umbilical Veins / cytology
Chemical
Reg. No./Substance:
0/Biological Markers; 0/CXCL12 protein, human; 0/CXCR4 protein, human; 0/Chemokine CXCL12; 0/Receptors, CXCR4

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


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