Decreased number of circulating CD34+KDR+ cells in asymptomatic subjects with preclinical atherosclerosis

Chironi, Gilles; Walch, Laurence; Pernollet, Marie-Gabrielle; Gariepy, Jérôme; Levenson, Jaime; Rendu, Francine; Simon, Alain

doi:10.1016/j.atherosclerosis.2006.02.041

Cited by 77 publications

(61 citation statements)

References 21 publications

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“…Published clinical studies on cardiovascular disease have often focused on surface expression for CD34 and VEGFR2 within the lymphocyte region by reporting low EPC frequency of around 0.01% of total mononuclear cells (6,10,(19)(20)(21). However, these studies differ methodologically in exclusion of dead cells and CD45…”

Section: Original Articlementioning

confidence: 99%

An optimized flow cytometry protocol for analysis of angiogenic monocytes and endothelial progenitor cells in peripheral blood

et al. 2009

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Circulating adult CD341 VEGFR2 1 endothelial progenitor cells (EPCs) have been shown to differentiate into endothelial cells, thus contributing to vascular homeostasis. Furthermore, a subset of circulating CD141 monocytes coexpresses CD16 together with the angiopoietin receptor Tie2 and has been functionally implicated in tumor angiogenesis. However, clinically applicable protocols for flow cytometric quantification of EPCs and Tie2 1 monocytes in peripheral blood and a consensus on reference values remain elusive. The number of Tie2 1 CD14 1 CD16 mid angiogenic monocytes and CD34 1 VEGFR2 1 CD45 low/2 EPCs was assessed in the peripheral venous blood of patients with stable coronary artery disease by three-color flow cytometry using specific monoclonal antibodies conjugated to PerCP, PE, PE-Cy7, APC, and APC-Cy7. Scatter multigating with exclusion of dead cells was performed to dissect complex mononuclear cell populations. This analysis was further refined by matching bright fluorochromes (PE-Cy7, PE, APC) with dimly expressed markers (CD34, VEGFR2, Tie2), by automatic compensation for minimizing fluorescence spillover and by using fluorescence-minus-one (FMO) controls to determine positive/negative boundaries. Presuming a Gaussian distribution, we obtained average values (mean AE SD) of 1.45 AE 1.29% for Tie2 1 CD14 1 CD16 mid monocytes (n ¼ 11, range: 0.12-3.64%) and 0.019 AE 0.013% for CD34low/2 EPCs (n ¼ 17, range: 0.003-0.042%). The intra-and inter-assay variability was 1.6% and 4.5%, respectively. We have optimized a fast and sensitive assay for the flow cytometric quantification of circulating angiogenic monocytes and EPCs in cardiovascular medicine. This protocol may represent a basis for standardized analysis and monitoring of these cell subsets to define their normal range and prognostic/diagnostic value in clinical use. ' 2009 International Society for Advancement of Cytometry

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Section: Original Articlementioning

confidence: 99%

An optimized flow cytometry protocol for analysis of angiogenic monocytes and endothelial progenitor cells in peripheral blood

et al. 2009

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“…The clinical relevance of EPC numbers was brought to the forefront cardiovascular risk prognostication when EPC numbers were shown to correlate positively with flow mediated brachial artery reactivity (a measure of endothelial function) and inversely with the Framingham risk score (Hill, Zalos et al 2003;Ghani, Shuaib et al 2005;Chironi, Walch et al 2007). Endothelial dysfunction observed in patients with cardiovascular disease or its risk factors may reflect a depressed ability to "renew" the endothelium from the circulating pool of EPCs which act to restore endothelial function.…”

Section: Endothelial Progenitor Cells and Atherosclerosismentioning

confidence: 99%

“…In asymptomatic individuals, EPC numbers correlate with the number of vascular beds with subclinical disease. In a study using ultrasound to characterize disease in the carotid artery, abdominal aorta and femoral artery, the number of EPCs cells was shown to be decreased stepwise in patients with plaque in 0, 1, 2 and 3 of the sites (Chironi, Walch et al 2007). Further, EPC numbers correlate with cardiovascular disease surrogates such as carotid intima-media thickness even after correction for the Framingham risk score and C-reactive protein (Fadini, Coracina et al 2006).…”

Section: Endothelial Progenitor Cells and Atherosclerosismentioning

confidence: 99%

“…Moreover, EPC numbers respond to risk factor modification and thus www.intechopen.com may provide a dynamic assessment of cardiovascular risk. EPC numbers correlate directly with endothelial function and inversely with Framingham risk score in asymptomatic individuals (Hill, Zalos et al 2003;Ghani, Shuaib et al 2005;Chironi, Walch et al 2007). EPC numbers correlate inversely with the number of vascular beds with subclinical disease in asymptomatic patients (Chironi, Walch et al 2007) and with cardiovascular disease surrogates such as carotid intima-media thickness after correction for the Framingham risk score and CRP (Fadini, Coracina et al 2006).…”

Section: Conclusion: a Paradigm For Cardiovascular Risk Assessmentmentioning

confidence: 99%

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Endothelial Progenitor Cell Number: A Convergence of Cardiovascular Risk Factors

Hoenig¹,

Sellke²

2012

Cardiovascular Risk Factors

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“…None of the markers used is specific of the EPCs. A combination of endothelial and hematopoietic markers can be also used, such as CD133, CD34, CD14, CD45, and KDR (Shintani et al, 2001;Urbich and Dimmeler, 2004;Valgimigli et al, 2004;Elsheikh et al, 2005;Chironi et al, 2006). Most studies have used CD34 + KDR + double positivity to quantify EPCs.…”

Section: Assessment Of Epc Numbers and Quantification In The Clinicalmentioning

confidence: 99%

Endothelial progenitor cells: Characterization, in vitro expansion, and prospects for autologous cell therapy

et al. 2007

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Injection of hematopoietic stem cells or endothelial progenitor cells (EPCs) expanded ex vivo has been shown to augment neovascularization in adult patients, but the precise origin and identity of the cell population responsible for these clinical benefits are controversial. The limited quantity of EPCs in the circulation has been the main obstacle to clinical trials. Several authors have therefore attempted to expand these cells ex vivo in order to obtain a homogeneous cell therapy product. One possible means of expanding EPCs ex vivo is to activate the thrombin receptor PAR-1 with the specific peptide SFLLRN. Indeed, PAR-1 activation promotes cell proliferation and C-X-C chemokine receptor type 4 (CXCR4) dependent migration and differentiation, with an overall angiogenic effect. This review summarizes the results and rationale of clinical trials of angiogenic therapy, the nature of EPCs, the different methods of ex vivo expansion, and current methods of quantification.

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Decreased number of circulating CD34+KDR+ cells in asymptomatic subjects with preclinical atherosclerosis

Cited by 77 publications

References 21 publications

An optimized flow cytometry protocol for analysis of angiogenic monocytes and endothelial progenitor cells in peripheral blood

An optimized flow cytometry protocol for analysis of angiogenic monocytes and endothelial progenitor cells in peripheral blood

Endothelial Progenitor Cell Number: A Convergence of Cardiovascular Risk Factors

Endothelial progenitor cells: Characterization, in vitro expansion, and prospects for autologous cell therapy

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