scholarly journals Probucol protects circulating endothelial progenitor cells from ambient PM2.5 damage via inhibition of reactive oxygen species and inflammatory cytokine production in�vivo

2018 ◽  
Author(s):  
Yong Chen ◽  
Ke Hu ◽  
Haoran Bu ◽  
Zhihua Si ◽  
Haihui Sun ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Oxygen Species ◽  
Endothelial Progenitor ◽  
Inflammatory Cytokine Production ◽  
Circulating Endothelial Progenitor Cells

Soluble CD40 ligand impairs the anti-platelet function of peripheral blood angiogenic outgrowth cells via increased production of reactive oxygen species

2013 ◽  
Vol 109 (05) ◽  
pp. 940-947 ◽  
Author(s):  
Lara Khzam ◽  
Ahmed Hachem ◽  
Younes Zaid ◽  
Rahma Boulahya ◽  
Walid Mourad ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Platelet Aggregation ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Platelet Function ◽  
Peripheral Blood ◽  
Reactive Oxygen ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Endothelial Progenitor

SummaryAdult peripheral blood angiogenic early outgrowth cells (EOCs), also known as early endothelial progenitor cells, interact with other blood and vascular cells and may regulate atherothrombosis. We have previously shown that endothelial progenitor cells inhibit platelet function and thrombus formation. The CD40L/CD40 axis is a thrombo-inflammatory mediator that affects platelet and endothelial functions. It has been shown that EOCs express CD40, whereas platelets represent the major source of its soluble ligand (sCD40L), which impairs EOC function. We aimed to test the hypothesis that the sCD40L/CD40 axis affects the anti-platelet function of EOCs. Human peripheral blood mononuclear cell-derived EOCs in culture inhibited platelet aggregation. Pre-treatment of EOCs with sCD40L reduced their in-hibitory effect on platelet aggregation in a CD40-dependent manner. EOCs viability and release of the anti-aggregating agents, prostacyclin and nitric oxide, were not affected by sCD40L. However, production of reactive oxygen species (ROS) was increased in sCD40L–treated EOCs. Blockade of ROS reversed the effects of sCD40L–treated EOCs on platelet aggregation. This study reveals that the sCD40L/CD40 axis impairs the anti-platelet properties of EOCs through increased production of ROS. These data may explain the link between elevated levels of sCD40L, impaired activity of EOCs and enhanced platelet reactivity, and consequently the occurrence of atherothrombotic disease.

scholarly journals Enzyme-Aided Extraction of Fucoidan by AMG Augments the Functionality of EPCs through Regulation of the AKT/Rheb Signaling Pathway

Marine Drugs ◽  
2019 ◽  
Vol 17 (7) ◽  
pp. 392
Author(s):  
Vinoth Kumar Rethineswaran ◽  
Yeon-Ju Kim ◽  
Woong Bi Jang ◽  
Seung Taek Ji ◽  
Songhwa Kang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Wound Healing ◽  
Cell Migration ◽  
Progenitor Cells ◽  
Signaling Pathway ◽  
Endothelial Progenitor Cells ◽  
Bioactive Compounds ◽  
Tube Formation ◽  
Oxygen Species ◽  
Endothelial Progenitor

The purpose of the present study is to improve the endothelial progenitor cells (EPC) activation, proliferation, and angiogenesis using enzyme-aided extraction of fucoidan by amyloglucosidase (EAEF-AMG). Enzyme-aided extraction of fucoidan by AMG (EAEF-AMG) significantly increased EPC proliferation by reducing the reactive oxygen species (ROS) and decreasing apoptosis. Notably, EAEF-AMG treated EPCs repressed the colocalization of TSC2/LAMP1 and promoted perinuclear localization of mTOR/LAMP1 and mTOR/Rheb. Moreover, EAEF-AMG enhanced EPC functionalities, including tube formation, cell migration, and wound healing via regulation of AKT/Rheb signaling. Our data provided cell priming protocols to enhance therapeutic applications of EPCs using bioactive compounds for the treatment of CVD.

Abstract 669: ET A Receptor Activation and ET B Receptor Deficiency Reduce Circulating Endothelial Progenitor Cells in Salt-Sensitive Hypertension

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Dan-Dan Chen ◽  
Xiao-Ling Dai ◽  
Melissa W Li ◽  
James J Galligan ◽  
Gregory D Fink ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Receptor Activation ◽  
Endothelial Progenitor ◽  
Circulating Endothelial Progenitor Cells ◽  
In Vivo Treatment ◽  
Salt Sensitive Hypertension

Background: Circulating endothelial progenitor cells (EPCs) are reduced in hypertension that correlates inversely with its mortality, but the mechanisms are poorly understood. DOCA-salt and ET B receptor deficiency rats (ET B −/ −) have salt-sensitive hypertension, characterized by increased ET-1 and oxidative stress levels. We hypothesized that ET A receptor activation and ET B receptor deficiency reduce circulating EPCs in adult male DOCA-salt rats. Methods and Results: Systolic blood pressure (SBP) was higher in DOCA-salt (4-wk regimen) vs. Sham rats (199.3 ± 4.8 vs. 133.4 ± 4.6 mmHg, n =8 –15, p<.05), which was significantly reduced by in vivo treatment with ET A antagonist ABT-627 (5 mg/kg/d) or NADPH oxidase inhibitor apocynin (1.5 mmol/L) (167.8 ± 6.8 and 156.9 ± 16.6 mmHg, respectively). Flow cytometry showed that circulating CD34- and Flk-1-positive EPCs were significantly lower in DOCA vs. Sham rats (31.5 ± 0.2 vs. 18.3 ± 0.8% and 21.1 ± 0.9 vs. 16.3 ± 0.7%, respectively, n=7– 8, p<.05). Dil-acLDL and isolectin double-stainings also showed reduced EPCs in DOCA vs. Sham rats (4.5 ± 0.4 vs. 10.2 ± 0.3 cells/hpf, n=5–15, p<.01), which was rescued by in vivo treatment with ABT-627 (10.1 ± 1.7) or apocynin (8.9 ± 0.8). Real-time RT-PCR and fluorescence confocal microscopy showed that ET A and ET B receptor mRNA and proteins were present in EPCs of SD rats. Intracellular ROS level was increased by >50% in EPCs of DOCA vs. Sham rats (DCF fluorescence, n = 9 –11, p<.05). Apoptosis was increased by >80% in EPCs of DOCA vs. Sham rats, which was reversed by ABT-627 or apocynin (TUNEL assay, n=5– 6, p<.05). EPCs were significantly lower in ET B −/ − vs. ET B +/+ rats (6.3 ± 0.6 cells/hpf, n =7– 8), paralleled with higher SBP (telemetry 151 ± 1.2 vs. 129 ± 0.9 mmHg, n = 6), plasma ET-1 level (5.2 ± 0.3 vs. 3.6 ± 0.1 pg/ml, n = 5–12), and suppressed telomerase activity (354.6 ± 105.5 vs. 83.3 ± 26.2%, n = 3) (all p<.05). ET-1 treatment (10 nM, 48 hrs) also reduced EPCs of normal rats (6.9 ± 0.1 vs. 10.3 ± 0.3 cells/hpf, n = 5– 6, p<.05), which was rescued by ABT-627 (9.9 ± 0.3), but not by ET B antagonist BQ788 (7.6 ± 0.4). Conclusion: ET A activation and ET B deficiency reduce circulating EPCs in DOCA-salt and ET B −/ − rats, in part, due to NADPH oxidase-induced oxidative stress, apoptosis, and telomerase inactivation.

Unresolved questions, changing definitions, and novel paradigms for defining endothelial progenitor cells

Blood ◽  
2005 ◽  
Vol 106 (5) ◽  
pp. 1525-1531 ◽  
Author(s):  
David A. Ingram ◽  
Noel M. Caplice ◽  
Mervin C. Yoder
Keyword(s):  
Endothelial Cells ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Circulating Endothelial Cells ◽  
Proliferative Potential ◽  
Endothelial Progenitor ◽  
Detailed Understanding ◽  
Circulating Endothelial Progenitor Cells

Abstract The field of vascular biology has been stimulated by the concept that circulating endothelial progenitor cells (EPCs) may play a role in neoangiogenesis (postnatal vasculogenesis). One problem for the field has been the difficulty in accurately defining an EPC. Likewise, circulating endothelial cells (CECs) are not well defined. The lack of a detailed understanding of the proliferative potential of EPCs and CECs has contributed to the controversy in identifying these cells and understanding their biology in vitro or in vivo. A novel paradigm using proliferative potential as one defining aspect of EPC biology suggests that a hierarchy of EPCs exists in human blood and blood vessels. The potential implications of this view in relation to current EPC definitions are discussed.

scholarly journals Dysfunction of endothelial progenitor cells in hyperlipidemic rats involves the increase of NADPH oxidase derived reactive oxygen species production

2017 ◽  
Vol 95 (5) ◽  
pp. 474-480 ◽  
Author(s):  
Ting-Bo Li ◽  
Jie-Jie Zhang ◽  
Bin Liu ◽  
Xiu-Ju Luo ◽  
Qi-Lin Ma ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Plasma Lipids ◽  
Reactive Oxygen ◽  
The Body ◽  
Ros Production ◽  
Oxygen Species ◽  
Endothelial Progenitor

NADPH oxidase (NOX) is a major source of reactive oxygen species (ROS) in the body and it plays a key role in mediation of oxidative injury in the cardiovascular system. The purposes of this study are to evaluate the status of NOX in endothelial progenitor cells (EPCs) of hyperlipidemic rats and to determine whether NOX-derived ROS promotes the dysfunction of EPCs. The rats were fed on a high-fat diet for 8 weeks to establish a hyperlipidemic rat model, which showed the increased plasma lipids and the impaired functions of circulating EPCs (including the reduced abilities in migration and adhesion) accompanied by an increase in NOX activity and ROS production. Next, EPCs were isolated from normal rats and they were treated with oxidized low-density lipoprotein (ox-LDL) (100 μg/mL) for 24 h to induce a dysfunctional model in vitro. In agreement with our findings in vivo, ox-LDL treatment increased the dysfunctions of EPCs concomitant with an increase in NOX activity and ROS production; these phenomena were reversed by the NOX inhibitor. Based on these observations, we conclude that NOX-derived ROS involved in the dysfunctions of circulating EPCs in hyperlipidemic rats and inhibition of NOX might provide a novel strategy to improve EPC functions in hyperlipidemia.

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