Oxidative stress impairs endothelial progenitor cell function

被引:95
作者
Case, Jamie [1 ]
Ingram, David A. [1 ,2 ]
Haneline, Laura S. [1 ,3 ]
机构
[1] Indiana Univ, Sch Med, Herman B Wells Ctr Pediat Res, Dept Pediat, Indianapolis, IN 46202 USA
[2] Indiana Univ, Sch Med, Dept Biochem & Mol Biol, Indianapolis, IN 46202 USA
[3] Indiana Univ, Sch Med, Dept Microbiol & Immunol, Indianapolis, IN 46202 USA
关键词
D O I
10.1089/ars.2008.2118
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:1895 / 1907
页数:13
相关论文
共 116 条
[1]   Role of redox potential and reactive oxygen species in stress signaling [J].
Adler, V ;
Yin, ZM ;
Tew, KD ;
Ronai, Z .
ONCOGENE, 1999, 18 (45) :6104-6111
[2]   Inhibition of NAD(P)H oxidase activity blocks vascular endothelial growth factor overexpression and neovascularization during ischemic retinopathy [J].
Al-Shabrawey, M ;
Bartoli, M ;
El-Remessy, AB ;
Platt, DH ;
Matragoon, S ;
Behzadian, MA ;
Caldwell, RW ;
Caldwall, RB .
AMERICAN JOURNAL OF PATHOLOGY, 2005, 167 (02) :599-607
[3]  
[Anonymous], 2005, National diabetes fact sheet
[4]   Isolation of putative progenitor endothelial cells for angiogenesis [J].
Asahara, T ;
Murohara, T ;
Sullivan, A ;
Silver, M ;
vanderZee, R ;
Li, T ;
Witzenbichler, B ;
Schatteman, G ;
Isner, JM .
SCIENCE, 1997, 275 (5302) :964-967
[5]  
BOUVIER CA, 1970, THROMB DIATH HAEMOST, P163
[6]   Gestational diabetes mellitus [J].
Buchanan, TA ;
Xiang, AH .
JOURNAL OF CLINICAL INVESTIGATION, 2005, 115 (03) :485-491
[7]   Endothelial dysfunction in cardiovascular diseases - The role of oxidant stress [J].
Cai, H ;
Harrison, DG .
CIRCULATION RESEARCH, 2000, 87 (10) :840-844
[8]   Hyperglycemia-induced reactive oxygen species and impaired endothelial progenitor cell function [J].
Callaghan, MJ ;
Ceradini, DJ ;
Gurtner, GC .
ANTIOXIDANTS & REDOX SIGNALING, 2005, 7 (11-12) :1476-1482
[9]   Human CD34+AC133+VEGFR-2+ cells are not endothelial progenitor cells but distinct, primitive hematopoietic progenitors [J].
Case, Jamie ;
Mead, Laura E. ;
Bessler, Waylan K. ;
Prater, Daniel ;
White, Hilary A. ;
Saadatzadeh, M. Reza ;
Bhavsar, Janak R. ;
Yoder, Mervin C. ;
Haneline, Laura S. ;
Ingram, David A. .
EXPERIMENTAL HEMATOLOGY, 2007, 35 (07) :1109-1118
[10]   RETRACTED: Number and activity of endothelial progenitor cells from peripheral blood in patients with hypercholesterolaemia (Retracted Article. See vol 119, pg 545, 2010) [J].
Chen, JZ ;
Zhang, FR ;
Tao, QM ;
Wang, XX ;
Zhu, JH ;
Zhu, JH .
CLINICAL SCIENCE, 2004, 107 (03) :273-280