Remnant-Like Lipoproteins May Accelerate Endothelial Progenitor Cells Senescence Through Inhibiting Telomerase Activity via the Reactive Oxygen Species-Dependent Pathway

2011 ◽  
Vol 27 (5) ◽  
pp. 628-634 ◽  
Author(s):  
De-guang Yang ◽  
Ling Liu ◽  
Sheng-hua Zhou ◽  
Mei-fang Ma ◽  
Tie Wen
Keyword(s):  
Reactive Oxygen Species ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Reactive Oxygen ◽  
Telomerase Activity ◽  
Oxygen Species ◽  
Endothelial Progenitor ◽  
Dependent Pathway

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 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.

Reactive Oxygen Species Might Have Important Roles On Angiogenesis of Endothelial Progenitor Cells Derived From HCB(Human Cord Blood) Which Are Stimulated by VEGF.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 1445-1445
Author(s):  
Eun-Sun Yoo ◽  
Yeung-Chul Mun ◽  
Kyoung-Eun Lee ◽  
Eunmi Nam ◽  
Jee-Young Ahn ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Reactive Oxygen ◽  
Tube Formation ◽  
Control Group ◽  
Oxygen Species ◽  
Endothelial Progenitor

Abstract Abstract 1445 Poster Board I-468 Purpose VEGF is a key angiogenic growth factor stimulating proliferation, migration, and tube formation on endothelial cells (ECs), that works through the VEGF receptor type 2 (VEGR2, KDR/Flk1). Reactive oxygen species (ROS) such as superoxide and H2O2 have roles signaling for molecules on angiogenesis. In present study, the aim is to investigate the roles of reactive oxygen species on neovascularization in endothelial progenitor cells. Methods Mononuclear cells isolated from UCB were cultured using EGM-2 medium with VEGF, IGF-1 and FGF or basal medium in presence or absence of VEGF for 7 days. Outgrowing endothelail progenitor cells (Yoo et al, STEM CELLS 21:228-235, 2003) at first week of culture were analyzed ROS production by dichlorofluorescein (DCF) fluorescence by use of 2,7-dichlorodihydro-fluoresceine-diacetate (H2DCF-DA). In order to determine that ROS production might involve in EPC proliferation and migration, we had analyzed the impact of N-acetyl-L-cysteine (NAC), broad spectrum ROS scavenger, and NAD(P)H oxidase inhibitor, diphenylene iodonium (DPI) using the proliferation, in vitro tube formation matrigel assay, migration assay with SDF-1/VEGF. We also analyzed the expression of NOX2-based NADPH oxidase (gp91phox) and activation of ERK2 and Akt (Thr308 and Ser473) using VEGF with or without DPI. Results Intracellular ROS level were increased during endothelial progenitor cell culture and were higher in UCB compared to that of BM and increased by VEGF treatment. Proliferation, in vitro tube formation matrigel assay and migration assay on endothelial progenitor cells using SDF-1/VEGF were decreased with additions of ROS scavenger DPI when compared with that of control group. In western blot data, NOX2-based NADPH oxidase(gp91phox) was increased by VEGF and decreased by addition of DPI. VEGF induced pERK2 expression was also decreased by DPI and that finding was correlated on down-regulation of endothelial cell proliferation by DPI. Activation of Ser473 Akt was found in control group and decreased by VEGF and rebounded by VEGF and DPI. But Thr308 Akt was not activated in our experiments. Conclusions These results suggested that NOX2-based NADPH oxidase(gp91phox)-induced ROS might play important roles on EPCs migration and proliferation by VEGF. Namely, manipulating the level of ROS biochemically may alter the pathogenesis in cardiovascular and in ischemic limb diseases. In results, these data may be useful to develop new therapeutic strategies. Disclosures No relevant conflicts of interest to declare.

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.

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