WO6-OR-3 ENDOTHELIAL PROGENITOR CELLS AND ENDOTHELIAL-DERIVED MICROPARTICLES IN HYPERTRIGLYCERIDEMIA: THE EFFECT OF THE METABOLIC SYNDROME

2007 ◽  
Vol 8 (1) ◽  
pp. 6
Author(s):  
M.R. Mannarino ◽  
M. Pirro ◽  
F. Bagaglia ◽  
C. Menecali ◽  
R. Paltriccia ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Endothelial Progenitor ◽  
The Metabolic Syndrome

scholarly journals Dysfunctional Endothelial Progenitor Cells in Metabolic Syndrome

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Sridevi Devaraj ◽  
Ishwarlal Jialal
Keyword(s):  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
Endothelial Dysfunction ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Disease Risk ◽  
Angiotensin Receptor Blockers ◽  
Endothelial Progenitor ◽  
The Metabolic Syndrome ◽  
Increased Risk

The metabolic syndrome (MetS) is highly prevalent and confers an increased risk of diabetes and cardiovascular disease. A key early event in atherosclerosis is endothelial dysfunction. Numerous groups have reported endothelial dysfunction in MetS. However, the measurement of endothelial function is far from optimum. There has been much interest recently in a subtype of progenitor cells, termed endothelial progenitor cells (EPCs), that can circulate, proliferate, and dfferentiate into mature endothelial cells. EPCs can be characterized by the assessment of surface markers, CD34 and vascular endothelial growth factor receptor-2, VEGFR-2 (KDR). The CD34+KDR+phenotype has been demonstrated to be an independent predictor of cardiovascular outcomes. MetS patients without diabetes or cardiovascular diseases have decreased EPC number and functionality as evidenced by decreased numbers of colony forming units, decreased adhesion and migration, and decreased tubule formation. Strategies that have been shown to upregulate and enhance EPC number and functionality include statins, angiotensin converting enzyme inhibitors, angiotensin receptor blockers, and peroxisome-proliferator-activating-receptor gamma agonists. Mechanisms by which they affect EPC number and functionality need to be studied. Thus, EPC number and/or functionality could emerge as novel cellular biomarkers of endothelial dysfunction and cardiovascular disease risk in MetS.

Endothelial progenitor cells are reduced in the metabolic syndrome and normalize after lipid-lowering therapy

2006 ◽  
Vol 45 (3) ◽  
pp. e27
Author(s):  
Peter E Westerweel ◽  
Jobien K Olijhoek ◽  
Imo E Hoefer ◽  
Gideon R Hajer ◽  
Olivia van Oostrom ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Lipid Lowering ◽  
Lipid Lowering Therapy ◽  
Endothelial Progenitor ◽  
The Metabolic Syndrome ◽  
Lowering Therapy

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.

scholarly journals Metabolic syndrome and nonalcoholic fatty liver disease. The role of endothelial progenitor cells♦

2013 ◽  
Vol 12 (6) ◽  
pp. 908-914 ◽  
Author(s):  
Ylse Gutiérrez-Grabe ◽  
Juan G. Gavilanes-Espinar ◽  
Felipe A. Masso-Rojas ◽  
Vicente Sánchez-Valle ◽  
Araceli Páez-Arenas ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Fatty Liver Disease ◽  
Endothelial Progenitor ◽  
Nonalcoholic Fatty Liver

Effects of insulin resistance on endothelial progenitor cells and vascular repair

2009 ◽  
Vol 117 (5) ◽  
pp. 173-190 ◽  
Author(s):  
Richard M. Cubbon ◽  
Matthew B. Kahn ◽  
Stephen B. Wheatcroft
Keyword(s):  
Insulin Resistance ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Endothelial Damage ◽  
Glucose Disposal ◽  
No Production ◽  
Vascular Repair ◽  
Endothelial Progenitor ◽  
The Metabolic Syndrome ◽  
Underlying Mechanisms

Insulin resistance, a key feature of obesity, the metabolic syndrome and Type 2 diabetes mellitus, results in an array of metabolic and vascular phenomena which ultimately promote the development of atherosclerosis. Endothelial dysfunction is intricately related to insulin resistance through the parallel stimulatory effects of insulin on glucose disposal in metabolic tissues and NO production in the endothelium. Perturbations characteristic of insulin resistance, including dyslipidaemia, inflammation and oxidative stress, may jeopardize the structural or functional integrity of the endothelium. Recent evidence suggests that endothelial damage is mitigated by endogenous reparative processes which mediate endothelial regeneration. EPCs (endothelial progenitor cells) are circulating cells which have been identified as mediators of endothelial repair. Several of the abnormalities associated with insulin resistance, including reduced NO bioavailability, increased production of ROS (reactive oxygen species) and down-regulation of intracellular signalling pathways, have the potential to disrupt EPC function. Improvement in the number and function of EPCs may contribute to the protective actions of evidence-based therapies to reduce cardiometabolic risk. In the present article, we review the putative effects of insulin resistance on EPCs, discuss the underlying mechanisms and highlight potential therapeutic manoeuvres which could improve vascular repair in individuals with insulin resistance.

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