scholarly journals Endothelial progenitor cells in pregnancy

Reproduction ◽  
2007 ◽  
Vol 133 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Amy O Robb ◽  
Nicholas L Mills ◽  
David E Newby ◽  
Fiona C Denison
Keyword(s):  
Endothelial Dysfunction ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Progenitor Cell ◽  
Mononuclear Cells ◽  
Vascular System ◽  
Specific Reference ◽  
Vascular Repair ◽  
Endothelial Progenitor ◽  
Cell Numbers

The discovery of endothelial progenitor cells has generated considerable interest in the field of vascular biology. These cells arise from a population of circulating mononuclear cells and have the capacity to form new blood vessels and contribute to vascular repair. Circulating endothelial progenitor cell numbers are reduced in patients with cardiovascular risk factors and in the presence of endothelial dysfunction, but are increased in response to ischaemia, oestrogens and drug therapy. They have been studied in pathologies from cardiovascular and renal disease to rheumatoid arthritis and pre-eclampsia. Pregnancy is a challenge to the maternal vascular system, requiring systemic adaptation and pronounced local changes in the uterus. Diseases of pregnancy such as pre-eclampsia and gestational diabetes increase the risk of pregnancy complications and are associated with endothelial dysfunction. We propose that endothelial progenitor cells have an important role in the regulation and maintenance of the vasculature during pregnancy. This review summarises our current understanding of endothelial progenitor cells, with specific reference to their role in angiogenesis and human pregnancy.

scholarly journals Effects of adrenomedullin on the cell numbers and apoptosis of endothelial progenitor cells

2008 ◽  
Vol 31 (3) ◽  
pp. 117 ◽  
Author(s):  
Xiang-Quan Kong ◽  
Le-Xin Wang ◽  
Chuan-Sheng Yang ◽  
Shuang-Feng Chen ◽  
Yu-Zeng Xue ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Mononuclear Cells ◽  
Gradient Centrifugation ◽  
Clinical Importance ◽  
Dependent Manner ◽  
Endothelial Progenitor ◽  
Concentration Dependent Manner ◽  
Pi3k Inhibitor Ly294002 ◽  
Cell Numbers

Purpose: To investigate the effect of adrenomedullin on the cell numbers and apoptosis of endothelial progenitor cells (EPCs). Methods: Mononuclear cells were isolated from peripheral blood by Ficoll density gradient centrifugation. The cells were stimulated with adrenomedullin, before and after the treatment of adrenomedullin-receptor antagonist, adrenomedullin 22-52, or a PI3K inhibitor LY294002. Results: Adrenomedullin dose-dependently increased the number of EPCs (P < 0.05). Adrenomedullin also significantly decreased apoptosis rate of EPCs in a concentration-dependent manner (P < 0.05). In the isolated human mononuclear cells pretreated with adrenomedullin 22-52 or LY294002, adrenomedullin failed to increase the number of EPCs or to reduce the level of apoptosis. Conclusions: Adrenomedullin increases the number of EPCs and decreases their apoptosis. These actions are likely mediated by PI3K signaling pathways. The clinical importance of these favourable effects on EPCs remains to be determined.

Presence of endothelial progenitor cells, distinct from mature endothelial cells, within human CD146+ blood cells

2005 ◽  
Vol 94 (12) ◽  
pp. 1270-1279 ◽  
Author(s):  
Bruno Delorme ◽  
Agnès Basire ◽  
Carla Gentile ◽  
Florence Sabatier ◽  
Frédéric Monsonis ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Network Formation ◽  
Mononuclear Cells ◽  
Circulating Endothelial Cells ◽  
Endothelial Progenitor ◽  
Color Flow ◽  
Immunodeficient Mice ◽  
Circulating Cells

SummaryCD146 is an adhesion molecule present on endothelial cells throughout the vascular tree. CD146 is also expressed by circulating endothelial cells (CECs) widely considered to be mature endothelial cells detached from injured vessels. The discovery of circulating endothelial progenitor cells (EPCs) originating from bone marrow prompted us to investigate whether CD146 circulating cells could also contains EPCs. We tested this hypothesis using an approach combining elimination of CECs by an adhesion step, followed by immunomagnetic sorting of remaining CD146+ cells from the non adherent fraction of cord blood mononuclear cells. When cultured under endothelial-promoting conditions, these cells differentiated as late outgrowth endothelial colonies: they grew as a cobblestone monolayer, were uniformly positive for endothelial markers and did not express leukocyte antigens. They highly proliferated and were expanded in long-term culture without alterations of their phenotypic and functional properties (DiI-ac-LDL uptake, wound repair, capillary-like network formation, and TNFα response). Moreover, these cells colonized a Matrigel plug in immunodeficient mice (NOD/SCID). Finally, using 4-color flow cytometry analysis of purified CD34+ cells, we clearly discriminated, CD146+ EPCs (CD146+ CD34+ CD45+ CD133+ or CD117+), and CD146+ CECs (CD146+ CD34+, CD45− CD133− or CD117−), both in cord and adult peripheral blood. The relative proportions of the two CD146+ subsets varied in patients with myocardial infarction as compared to healthy subjects. Our study establishes that, beside CECs, CD146+ circulating cells contain a subpopulation of EPCs with potential use in proangiogenic therapy. In addition, the dual measurement of CD146+ CECs and CD146+ EPCs offers a promising tool for monitoring vascular injury/regeneration processes in clinical situations.

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 Interleukin-1β Augments Angiogenic Responses of Murine Endothelial Progenitor Cells in Vitro

2009 ◽  
Vol 29 (5) ◽  
pp. 933-943 ◽  
Author(s):  
Anna Rosell ◽  
Ken Arai ◽  
Josephine Lok ◽  
Tongrong He ◽  
Shuzhen Guo ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Mononuclear Cells ◽  
Therapeutic Angiogenesis ◽  
Interleukin 1Β ◽  
Endothelial Progenitor ◽  
Angiogenic Potential ◽  
Diphenyl Tetrazolium Bromide ◽  
In Vitro Angiogenesis

Endothelial progenitor cells (EPCs) may provide novel opportunities for therapeutic angiogenesis after ischemic diseases. However, it is unclear how the angiogenic potential of EPCs might be affected by an inflammatory environment. We examine how the potent cytokine interleukin-1β (IL-1β) affects angiovasculogenic responses in EPCs in culture. Mononuclear cells isolated from mouse spleen were plated on fibronectin-coated wells and grown in EGM-2 MV media. Endothelial progenitor cells were phenotyped using multiple markers (UEA-Lectin, ac-LDL, CD133, CD34, vWillebrand Factor, Flk-1) and to identify the IL-1 Receptor-I. We quantified cell and colony counts and performed MTT (3-(4,5-dimethylthiazol-2-yl)2,5-diphenyl-tetrazolium bromide) and Matrigel assays, in vitro, under control and IL-1β (10 ng/mL) conditions. Endothelial progenitor cells exposed to IL-1β increased in the number of cells and colonies compared with untreated cells, without any effect on cell metabolic integrity. Furthermore, IL-1β treatment augmented EPC angiogenic function, significantly increasing the number of vessel-like structures in the Matrigel assay. An early phosphorylation of ERK1/2 occurred after IL-1β stimulation, and this pathway was inhibited if IL-1 Receptor-I was blocked. Our results suggest that IL-1β is a potent stimulator of in vitro angiogenesis through ERK signaling in mouse EPCs. Further studies are warranted to assess how interactions between proinflammatory environments and EPC responses may be leveraged to enhance therapeutic angiogenesis.

scholarly journals Does erythropoietin therapy affect circulating endothelial cells in hemodialysis patients?

2020 ◽  
pp. 29-37
Author(s):  
T. Bulduk ◽  
A. U. Yalcin ◽  
O. M. Akay ◽  
S. G. Ozkurt ◽  
H. U. Teke ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Endothelial Progenitor Cell ◽  
Peripheral Blood ◽  
Progenitor Cell ◽  
Hemodialysis Patients ◽  
Circulating Endothelial Cells ◽  
Control Group ◽  
Endothelial Progenitor

Anemia is a common complication of chronic kidney disease (CKD). The most common cause of anemia in CKD is erythropoietin deficiency; and the most important cause of mortality in CKD patients is atherosclerotic vascular complications which are associated with endothelial damage. One of the methods evaluating vascular integrity is the cytometric measurement of circulating endothelial cells and endothelial progenitor cells in peripheral blood. The study aimed to investigate the effects of erythropoietin therapy on endothelial dysfunction by evaluating circulating endothelial cells and endothelial progenitor cells in peripheral blood using the technique of flow cytometry. Methods. A total of 55 hemodialysis patients were evaluated in three groups; those having erythropoietin therapy for at least last 3 months (n = 20) / not having erythropoietin for at least the last 3 months (n = 20) and the patients who started erythropoietin treatment during the study (n = 5). The control group consisted of 20 people. Blood values of the 3rd Group were investigated three times as baseline, 2nd week and 8th week CD34 +, CD105 + cells were evaluated as activated circulating endothelial cells; CD133 +, CD146 + cells were evaluated as activated endothelial progenitor cells. Results. There was no difference between the patients and healthy individuals in terms of circulating endothelial cells and endothelial progenitor cells. In the third group, no differences were observed in circulating endothelial cells / endothelial progenitor cell levels at baseline / 2nd and 8th weeks. There was no correlation between erythropoietin and circulating endothelial cells / endothelial progenitor cells. Conclusion. A correlation is not available between the therapeutic doses of erythropoietin used in hemodialysis patients and circulating endothelial cells / endothelial progenitor cell levels; supratherapeutic doses could change the results.

scholarly journals Decreased Count and Dysfunction of Circulating EPCs in Postmenopausal Hypercholesterolemic Females via Reducing NO Production

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Ying Luo ◽  
Quan-Neng Yan ◽  
Wan-Zhou Wu ◽  
Fan-Yan Luo
Keyword(s):  
Endothelial Dysfunction ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Therapeutic Strategy ◽  
No Production ◽  
Endothelial Progenitor ◽  
Endothelial Repair ◽  
Flow Mediated Dilatation ◽  
Premenopausal Female ◽  
And Function

Endothelial progenitor cells (EPCs) contribute to the endogenous endothelial repair program during hypercholesterolemia. EPC count and migratory and proliferative capacities remain unchanged in the premenopausal female with hypercholesterolemia. However, the changes of count and activity of circulating EPCs in the hypercholesterolemic postmenopausal females are unknown. Here, we find that the migratory and proliferative capacities of circulating EPCs were decreased in patients with hypercholesterolemia versus normocholesterolemia. No significant differences were found between postmenopausal females and age-matched males. NO production showed positive correlation with the activity and count of circulating EPCs in patients with hypercholesterolemia. Flow-mediated dilatation (FMD) is directly interrelated with EPC counts and function. Our findings reveal that decreased EPC count and endothelial dysfunction lead to less NO production in hypercholesterolemic postmenopausal females. Maintaining the EPC numbers and activity might be emerging as a potential therapeutic strategy to reduce the risk of cardiovascular injury in elder women.

Abstract 3698: Decreased Circulating Endothelial Progenitor Cells and Endothelial Dysfunction: a Novel Mechanism of Atherogenesis in Obesity.

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Paulo F Leite ◽  
Claudia R Andrade ◽  
Santa Poppe ◽  
Luiz A Cesar ◽  
Silmara Coimbra ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Multivariate Analysis ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Obese Patients ◽  
Endothelial Progenitor ◽  
Circulating Endothelial Progenitor Cells ◽  
Morbid Obese

Underlying mechanisms of endothelial dysfunction in obesity are not fully understood. Circulating Endothelial Progenitor Cells (EPCs) are known to promote endothelial repair. Our aim was to assess the number/function of EPCs in morbid obese individuals and its correlation with endothelial function and inflammatory markers. EPCs were isolated from 33 morbid obese patients (age 47±1.8 y; men=34%; BMI=49±2.1 kg/m 2 , metabolic syndrome=84%) and 20 lean controls. Peripheral blood EPC number was significantly reduced in obese patients both with flow cytometry (KDR + /CD34 + ; 0.041±0.04 vs 0.074±0.05 %events, p<0.001) and fluorescence analysis after short-term culture (49±4 vs 28±2 cells/field, p<0.001). The plasma number of primitive CD 133 + cells, and concentrations of VEGF (Elisa) and nitrogen oxides (which potentially recruit EPCs), were similar to control, suggesting that reduction of EPCs occurs distally to early cell differentiation. Importantly, C-Reactive Protein (CRP), robustly increased in obese patients (0.15±0.04 vs 1.3±0.3; p=0.003), was a strong predictor of reduced EPC number at multivariate analysis (r=0.623; p < 0.001). Likewise, the migratory response of EPCs to VEGF in vitro was significantly impaired in obese vs controls, despite similar VEGF receptor numbers. Multivariate analysis suggested potential roles of metabolic syndrome and leptin in such effect. Endothelial function at flow-mediated brachial artery reactivity was markedly reduced (by 60%) in obese patients, and had a significant inverse correlation with EPC number (r= 0.678; p< 0.001). Carotid intimal thickness was also increased in obese patients (0.68±0.02 vs 0.58±0.08; p=0.001). On the other hand, the number of circulating endothelial cells (CD31 + /CD106 + ) was similar in both groups, suggesting that apoptosis was not enhanced in the obese. These results suggest for the first time that reduced number and migratory capacity of EPCs correlate with endothelial dysfunction or increased CRP and may be a key underlying mechanism of vascular complications and atherosclerosis in obesity.

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 Protective Effect of Silymarin against Rapamycin-induced Apoptosis and Proliferation Inhibition in Endothelial Progenitor Cells

2015 ◽  
Vol 10 (2) ◽  
pp. 1934578X1501000 ◽  
Author(s):  
Peng Zhang ◽  
Guohua Han ◽  
Pei Gao ◽  
Kun Qiao ◽  
Yusheng Ren ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Mononuclear Cells ◽  
Control Group ◽  
Dependent Manner ◽  
Endothelial Progenitor ◽  
Concentration Dependent Manner ◽  
Inhibition Of Proliferation ◽  
And Migration ◽  
Proliferation And Migration

For this study, peripheral blood samples were collected from human volunteers. Mononuclear cells (MNC) were separated by density centrifugation and were induced to differentiate into endothelial progenitor cells (EPCs) in vitro. Different concentrations of rapamycin and silymarin were introduced to the EPCs over 24 hours and then EPCs were analyzed for proliferation, migration, apoptosis and angiogenesis. Compared with the control group, rapamycin (1, 10, 100 ng/mL) inhibited the proliferation and migration of EPCs in a concentration dependent manner ( P<0.05). Silymarin (50, 100 μg/mL) enhanced the proliferation and migration of EPCs and inhibited apoptosis in a concentration dependent manner ( P<0.05). By adding rapamycin (1 ng/mL) and silymarin (25, 50, 100 μg/mL) over 24 hours, silymarin inhibited the pro-apoptotic effect of rapamycin on EPCs, and reversed the inhibition of proliferation, migration and angiogenesis of EPCs by rapamycin ( P<0.05).

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