Circulating CD34+ cell subsets in patients with coronary endothelial dysfunction

Boilson, Barry A.; Kiernan, Thomas J.; Harbuzariu, Adriana; Nelson, Rebecca E.; Lerman, Amir; Simari, Robert D.

doi:10.1038/ncpcardio1277

Cited by 50 publications

(45 citation statements)

References 35 publications

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“…These include genes that have been previously linked to atherosclerosis, such as Abcb4, Ctsk, Ptpn1, Ptpn6, Ptprc, and Msr1 (35)(36)(37)(38)(39)(40), and genes that we believe to be novel, like Atgr1a, Gpr65, Inpp5d, Mcoln2, Ctsz, Ptpre, Havcr2, and Galns. C3ar1, although not in the common plaque progression signature, is a G protein-coupled receptor and may also serve as a candidate drug target.…”

Section: Discussionmentioning

confidence: 98%

Identification and validation of genes affecting aortic lesions in mice

Yang¹,

Peterson²,

Thieringer³

et al. 2010

J. Clin. Invest.

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Atherosclerosis represents the most significant risk factor for coronary artery disease (CAD), the leading cause of death in developed countries. To better understand the pathogenesis of atherosclerosis, we applied a likeli hoodbased model selection method to infer genedisease causality relationships for the aortic lesion trait in a segregating mouse population demonstrating a spectrum of susceptibility to developing atherosclerotic lesions. We identified 292 genes that tested causal for aortic lesions from liver and adipose tissues of these mice, and we experimentally validated one of these candidate causal genes, complement component 3a receptor 1 (C3ar1), using a knockout mouse model. We also found that genes identified by this method overlapped with genes progressively regulated in the aortic arches of 2 mouse models of atherosclerosis during atherosclerotic lesion development. By comparing our gene set with findings from public human genomewide association studies (GWAS) of CAD and related traits, we found that 5 genes identified by our study overlapped with published studies in humans in which they were identified as risk factors for multiple atherosclerosisrelated pathologies, including myocardial infarction, serum uric acid levels, mean platelet volume, aortic root size, and heart failure. Candidate causal genes were also found to be enriched with CAD risk polymorphisms identified by the Wellcome Trust Case Control Consortium (WTCCC). Our findings therefore validate the ability of cau sality testing procedures to provide insights into the mechanisms underlying atherosclerosis development.

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Section: Discussionmentioning

confidence: 98%

Identification and validation of genes affecting aortic lesions in mice

Yang¹,

Peterson²,

Thieringer³

et al. 2010

J. Clin. Invest.

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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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“…It's a marker for hematopoietic stem cells (HSCs), endothelial progenitor cells (EPCs) & small vessels endothelium [5][6][7][8][9][10] .Paraffin sections were deparaffinized, rehydrated, incubated with hydrogen peroxide for 30 minutes then rinsed in PBS. Sections were incubated for one hour with 2 drops (=100 μl) of the primary antibody CD34 Ab-1, Clone QBEnd/10 (Lab Vision Corporation Laboratories, CA 94539, USA, catalogue number MS-363-R7).…”

Section: Evaluation Of the Morphological Changes Of Kidney After Ischmentioning

confidence: 99%

“…The two subsets of BMDCs expressing CD34 are hematopoietic stem cells (HSCs) & endothelial progenitor cells (EPCs) and are hypothesized to have a common precursor cell, hemangioblast [10] . Thus in this study,CD34 antibody was used as marker for the detection of both hematopoietic stem cells (HSCs) and endothelial progenitor cells (EPCs).…”

Section: Discusionmentioning

confidence: 99%

Role of Erythropoietin Induced Stem Cell Mobilization in the Repairing of Acute Kidney Injury Following Ischemia Reperfusion in Albino Rats: A Histological Study

Nada

Ahmed

Farag

et al. 2017

Journal of Medical Histology

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Background: The incidence of acute kidney injury (AKI), the new term for acute renal failure, has increased in recent years. Ischemia-reperfusion (IR) is one of the main causes of AKI. Erythropoietin (EPO) is a complex molecule, which regulates red blood cell production in the bone marrow. Recent studies provide evidence of potential therapeutic effect of EPO on AKI. Aim of the Work: Investigate the role of EPO in mobilization of bone marrow derived stem cells and its role in repairing AKI. Materials and Methods:This study included 32 adult male albino rats, divided into three groups; control, non-treated IR and EPO treated group. AKI was done by induction of IR via clamping both renal pedicles for 40 minutes and EPO 5000 U|kg was injected in treated group once intraperitoneally immediately after IR. Rats were sacrificed 48 hours and 1 week after intervention, then renal sections were stained with hematoxylin & eosin, PAS and immunohistochemically for CD34. Results: Erythropoietin improved the impaired kidney manifestations occurred by IR including increasing the reduced urea and creatinine levels, improved histological architecture of kidney. Also, increasing CD34 immunopositive hematopoietic and endothelial progenitor stem cells. Conclusion: This work concluded that administration of EPO at time of renal IR resulted in enhanced mobilization of stem cells resulting in structural recovery and improved functions.

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Circulating CD34+ cell subsets in patients with coronary endothelial dysfunction

Cited by 50 publications

References 35 publications

Identification and validation of genes affecting aortic lesions in mice

Identification and validation of genes affecting aortic lesions in mice

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

Role of Erythropoietin Induced Stem Cell Mobilization in the Repairing of Acute Kidney Injury Following Ischemia Reperfusion in Albino Rats: A Histological Study

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