Vascular Disease Risk in Patients With Hypertriglyceridemia: Endothelial Progenitor Cells, Oxidative Stress, Accelerated Senescence, and Impaired Vascular Repair

2011 ◽  
Vol 27 (5) ◽  
pp. 538-540 ◽  
Author(s):  
Eric Thorin
Keyword(s):  
Oxidative Stress ◽  
Vascular Disease ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Disease Risk ◽  
Vascular Repair ◽  
Endothelial Progenitor ◽  
Accelerated Senescence

Carbamylated low‐density lipoprotein induces oxidative stress and accelerated senescence in human endothelial progenitor cells

2011 ◽  
Vol 25 (4) ◽  
pp. 1314-1322 ◽  
Author(s):  
Julia Carracedo ◽  
Ana Merino ◽  
Carolina Briceño ◽  
Sagrario Soriano ◽  
Paula Buendía ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Endothelial Progenitor ◽  
Accelerated Senescence

Apurinic/apyrimidinic endonucelase 1 maintains adhesion of endothelial progenitor cells and reduces neointima formation

2013 ◽  
Vol 305 (8) ◽  
pp. H1158-H1167 ◽  
Author(s):  
Atsushi Yamauchi ◽  
Jun-ichi Kawabe ◽  
Maki Kabara ◽  
Motoki Matsuki ◽  
Akira Asanome ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Cellular Response ◽  
Neointima Formation ◽  
Vascular Repair ◽  
Endothelial Progenitor ◽  
Adhesion Properties ◽  
Vascular Walls

Apurinic/apyrimidinic endonuclease 1 (APE1) is a multifunctional protein that processes DNA-repair function and controls cellular response to oxidative stress. Endothelial progenitor cells (EPCs) are recruited to oxidative stress-rich injured vascular walls and positively contribute to vascular repair and endothelialization. We hypothesized that APE1 functions for EPCs-mediated inhibition of neointima formation in injured vasculature. EPCs isolated from bone marrow cells of C57BL6 mice (12–16 wk old) were able to survive in the presence of hydrogen peroxide (H2O2; up to 1,000 μM) due to the highly expressed reactive oxygen species (ROS) scavengers. However, adhesion capacity of EPCs was significantly inhibited by H2O2 (100 μM) even though an intracellular ROS was retained at small level. An APE1-selective inhibitor or RNA interference-mediated knockdown of endogenous APE1 in EPCs aggravated the H2O2-mediated inhibition of EPCs-adhesion. In contrast, when APE1 was overexpressed in EPCs using an adenovirus harboring the APE1 gene (APE-EPCs), adhesion was significantly improved during oxidative stress. To examine in vivo effects of APE1 in EPCs, APE-EPCs were transplanted via the tail vein after wire-mediated injury of the mouse femoral artery. The number of adherent EPCs at injured vascular walls and the vascular repair effect of EPCs were enhanced in APE-EPCs compared with control EPCs. Among the cellular functions of EPCs, adhesion is especially sensitive to oxidative stress. APE1 enhances in vivo vascular repair effects of EPCs in part through the maintenance of adhesion properties of EPCs. APE1 may be a novel and useful target gene for effective cellular transplantation therapy.

AB0147 Oxidative stress and flogosis: The role of endothelial progenitor cells in rheumathoid arthtritis

2013 ◽  
Vol 71 (Suppl 3) ◽  
pp. 646.1-646
Author(s):  
A. Lo Gullo ◽  
G. Mandraffino ◽  
A. Sardo ◽  
A. D’Ascola ◽  
E. Imbalzano ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Endothelial Progenitor

Intrinsic Vascular Repair by Endothelial Progenitor Cells in Acute Coronary Syndromes: an Update Overview

2018 ◽  
Vol 15 (1) ◽  
pp. 35-47 ◽  
Author(s):  
Vânia Leal ◽  
Carlos Fontes Ribeiro ◽  
Bárbara Oliveiros ◽  
Natália António ◽  
Sónia Silva
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Acute Coronary Syndromes ◽  
Vascular Repair ◽  
Endothelial Progenitor ◽  
Coronary Syndromes

scholarly journals Ox-LDL induced endothelial progenitor cells oxidative stress via p38/Keap1/Nrf2 pathway

2021 ◽  
Author(s):  
Qijun Jiang ◽  
Chengpeng Li ◽  
Zhigang Gong ◽  
Zhigang Li ◽  
Shifang Ding
Keyword(s):  
Oxidative Stress ◽  
Membrane Potential ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Nuclear Translocation ◽  
Tube Formation ◽  
Ros Generation ◽  
Endothelial Progenitor ◽  
Migration Ability ◽  
Nrf2 Pathway

Abstract Background In many studies, endothelial progenitor cells (EPCs) highly expressing antioxidant protein were induced oxidative stress and apoptosis by Oxidized-low density lipoprotein (ox-LDL). Nrf2 which was resently reported to regulate the antioxidant genes and cellular redox regulators was highly expressed in EPCs. However, its role in ox-LDL induced EPCs oxidative stress and apoptosis has not been fully illustrated. Methods EPCs isolated from human peripheral blood mononuclear cells were treated with different concentration of ox-LDL, Keap1 siRNA and a specific p38 MAPK inhibitor SB203580, then used to assay the whole cellular Nrf2 (total Nrf2, t-Nrf2), cytoplasmic Nrf2 (c-Nrf2), nuclear Nrf2 (n- Nrf2), NAD(P) H:quinone oxidoreductase 1 (NQO1) protein levels and Bax /Bcl-2 with western blot, NQO1 mRNA levels with RT-PCR, ROS level with H2DCF-DA, the loss/disruption of mitochondrial membrane potential (MMP) with JC-1, apoptosis with Annexin-V and PI,migration ability with transwell chambers and tube formation. Results The ox-LDL treatment decreased the n-Nrf2/Histone H3 to c-Nrf2/GAPDH ratio, NQO1 mRNA and protein expression levels. Treatment of ox-LDL enhanced the ROS production, induced loss of membrane potential, increase in cell shrinkage, pyknotic nuclei and apoptosis of EPCs. The Keap1 knockdown with Keap1 siRNA increased the nuclear translocation of Nrf2, the NQO1 mRNA and protein transcription levels, and prevented ox-LDL induced ROS generation and formation of JC-1 monomers. Treatment of ox-LDL increased the activation of p38. Pretreatment with SB203580 significantly eliminated ox-LDL induced the inhibition of Nrf2 nuclear translocation, the depression of the mRNA transcription levels of NQO-1, the ROS generation and the formation of JC-1 monomers in EPCs. The pretreatment of Keap1 siRNA decreased the Bax/Bcl-2 ratio which was increased by the treatment of ox-LDL in EPCs. The ox-LDL treatment decreased EPCs migration activity and tube formation. Whereas the pre-treatment with Keap1 siRNA preserved the migration ability and tube formation of EPCs Conclusion Ox-LDL induced EPCs oxidative stress and apoptosis via p38/Keap1/Nrf2 pathway.

Endothelial Progenitor Cells for Vascular Repair

2010 ◽  
pp. 297-320
Author(s):  
Melissa A. Brown ◽  
Cindy S. Cheng ◽  
George A. Truskey
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Vascular Repair ◽  
Endothelial Progenitor

scholarly journals Intravenous Administration of Allogenic Cell-Derived Microvesicles of Healthy Origins Defends Against Atherosclerotic Cardiovascular Disease Development by a Direct Action on Endothelial Progenitor Cells

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 423 ◽  
Author(s):  
Nicoleta Alexandru ◽  
Eugen Andrei ◽  
Florentina Safciuc ◽  
Emanuel Dragan ◽  
Ana Maria Balahura ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Vascular Disease ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Left Ventricular ◽  
Biologically Active ◽  
Atherosclerotic Cardiovascular Disease ◽  
Disease Development ◽  
Atherosclerotic Vascular Disease ◽  
Endothelial Progenitor

Atherosclerosis and cardiovascular disease development is the outcome of intermediate processes where endothelial dysfunction and vascular inflammation are main protagonists. Cell-derived microvesicles (MVs), endothelial progenitor cells (EPCs), and circulating microRNAs (miRNAs) are known as biomarkers and potential regulators for atherosclerotic vascular disease, but their role in the complexity of the inflammatory process and in the mechanism of vascular restoration is far from clear. We aimed to evaluate the biological activity and functional role of MVs, in particular of the EPCs-derived MVs (MVEs), of healthy origins in reducing atherosclerotic vascular disease development. The experiments were performed on hamsters divided into the following groups: simultaneously hypertensive–hyperlipidemic (HH group) by combining two feeding conditions for 4 months; HH with retro-orbital sinus injection containing 1 × 105 MVs or MVEs from control hamsters, one dose per month for 4 months of HH diet, to prevent atherosclerosis (HH-MVs or HH-MVEs group); and controls (C group), age-matched normal healthy animals. We found that circulating MV and MVE transplantation of healthy origins significantly reduces atherosclerosis development via (1) the mitigation of dyslipidemia, hypertension, and circulating EPC/cytokine/chemokine levels and (2) the structural and functional remodeling of arterial and left ventricular walls. We also demonstrated that (1) circulating MVs contain miRNAs; this was demonstrated by validating MVs and MVEs as transporters of Ago2-miRNA, Stau1-miRNA, and Stau2-miRNA complexes and (2) MV and MVE administration significantly protect against atherosclerotic cardiovascular disease via transfer of miR-223, miR-21, miR-126, and miR-146a to circulating late EPCs. It should be mentioned that the favorable effects of MVEs were greater than those of MVs. Our findings suggest that allogenic MV and MVE administration of healthy origins could counteract HH diet-induced detrimental effects by biologically active miR-10a, miR-21, miR-126, and miR-146a transfer to circulating EPCs, mediating their vascular repair function in atherosclerosis processes.

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