Document Detail

Oxidative stress impairs endothelial progenitor cell function.
MedLine Citation:
PMID:  18627346     Owner:  NLM     Status:  MEDLINE    
Circulating endothelial progenitor cells (EPCs) in adult human peripheral blood were identified in 1997. Since their original identification, EPCs have been extensively studied as biomarkers to assess the risk of cardiovascular disease in human subjects and as a potential cell therapeutic for vascular regeneration. EPCs are exposed to oxidative stress during vascular injury as residents of blood vessel walls or as circulating cells homing to sites of neovascularization. Given the links between oxidative injury, endothelial cell dysfunction, and vascular disease, recent investigation has focused on the responses of EPCs to oxidant stress and the molecular mechanisms that control redox regulation in these specialized cells. In this review, we discuss the various cell and flow-cytometric techniques used to define and isolate EPCs from circulating blood and the current human and mouse genetic data, which offer insights into redox control in EPC biology and angiogenesis. Finally, we review how EPC responses to oxidant stress may be a critical determinant in maintaining the integrity and function of the cardiovascular system and how perturbations of redox control in EPCs may lead to various human diseases.
Jamie Case; David A Ingram; Laura S Haneline
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review    
Journal Detail:
Title:  Antioxidants & redox signaling     Volume:  10     ISSN:  1557-7716     ISO Abbreviation:  Antioxid. Redox Signal.     Publication Date:  2008 Nov 
Date Detail:
Created Date:  2008-09-08     Completed Date:  2008-11-26     Revised Date:  2014-09-21    
Medline Journal Info:
Nlm Unique ID:  100888899     Medline TA:  Antioxid Redox Signal     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1895-907     Citation Subset:  IM    
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MeSH Terms
Endothelial Cells / cytology,  physiology*
Models, Biological
Neovascularization, Physiologic / physiology
Oxidative Stress / physiology*
Stem Cells / cytology,  physiology*
Vascular Diseases / physiopathology
Grant Support
1 K08 CA096579/CA/NCI NIH HHS; K08 CA096579-01/CA/NCI NIH HHS; K08 CA096579-02/CA/NCI NIH HHS; K08 CA096579-03/CA/NCI NIH HHS; K08 CA096579-04/CA/NCI NIH HHS; K08 CA096579-05/CA/NCI NIH HHS; K08 CA096579-06/CA/NCI NIH HHS; P30 CA82709/CA/NCI NIH HHS; P50 NS052606/NS/NINDS NIH HHS; P50 NS052606-010003/NS/NINDS NIH HHS; P50 NS052606-020003/NS/NINDS NIH HHS; P50 NS052606-030003/NS/NINDS NIH HHS; R01 HL077175/HL/NHLBI NIH HHS; R01 HL077175/HL/NHLBI NIH HHS; R01 HL077175-01A1/HL/NHLBI NIH HHS; R01 HL077175-02/HL/NHLBI NIH HHS; R01 HL077175-03/HL/NHLBI NIH HHS; R01 HL077175-04/HL/NHLBI NIH HHS; R21 HL088885/HL/NHLBI NIH HHS; R21 HL088885/HL/NHLBI NIH HHS; R21 HL088885-01/HL/NHLBI NIH HHS; R21 HL088885-02/HL/NHLBI NIH HHS

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