scholarly journals Circulating Endothelial Progenitor Cells and Endothelial Microparticles in Patients With Arterial Erectile Dysfunction and Metabolic Syndrome

2011 ◽  
Vol 33 (2) ◽  
pp. 202-209 ◽  
Author(s):  
S. La Vignera ◽  
R. Condorelli ◽  
E. Vicari ◽  
R. D'Agata ◽  
A. E. Calogero
Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Paulo F Leite ◽  
Claudia R Andrade ◽  
Santa Poppe ◽  
Luiz A Cesar ◽  
Silmara Coimbra ◽  
...  

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.


Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1819-1819
Author(s):  
Joaquin J. Jimenez ◽  
Alexander Ferreira ◽  
Hannah J. Dodson ◽  
Katherine M. Lens ◽  
Lucia M. Mauro ◽  
...  

Abstract INTRODUCTION: High cholesterol (HC) is known to adversely affect endothelial cells (EC) and has been shown to correlate with decreased levels of circulating endothelial progenitor cells (CEPC). We assayed endothelial microparticles (EMP), a sensitive indicator of EC perturbation, to investigate relations among HC, CEPC, and injury of coronary artery endothelial cells (CAEC), both in vivo and in vitro. METHODS: Twelve subjects with normal cholesterol (150 ±30 mg/dL, control) and 12 with HC (250 ±25) were studied. EMP were assayed by flow cytometry using fluorescent antibodies and CAEC were cultured as previously described [Jimenez et al, Thromb Res 109:175, 2003]. CEPC were isolated, cultured, and assayed for endothelial colony formation (CFU) as described [Hill et al, NEJM 348:593, 2003]. RESULTS: Comparing the two groups, EMP measured by CD31+/CD42b− were nearly 2.5-fold elevated in HC as compared to controls (1.7 ±0.5 ×106/mL vs.0.35 ±0.02 ×106/mL; p<0.01). Cholesterol levels correlated well with this measure of EMP (R=0.60, p=0.002). However, no significant correlation was found between CD62E+ EMP and cholesterol levels. Assay of CEPC revealed a nearly 2.5-fold decrease in CFU in HC vs. controls (10 ±2 vs. 25 ±4; p<0.01). In studies in vitro, CEPC from controls were cultured in presence of 20% 0.1μm filtered plasma from members of both groups. The HC group plasma inhibited CEPC colony formation by almost 50% (23 ±3.5 CFU for control plasma vs. 13 ±4 colonies for HC plasma). We next assessed the longer-term effect of HC plasma on CAEC cultures. Six-day culture of CAEC in the presence of 20% plasma resulted in a significant increase of CD31+/CD42b− EMP from CAEC treated with HC plasma vs. normal plasma (6.5 ±0.7 ×106/mL vs. 0.23 ±0.03 ×106/mL; p=0.02). CONCLUSION: These results suggest that EMP are useful markers to monitor cholesterol mediated-EC changes. High EMP levels inversely reflect the vascular endothelial cell regeneration potential due to decreased circulating endothelial progenitor cells.


Endocrine ◽  
2014 ◽  
Vol 49 (2) ◽  
pp. 415-421 ◽  
Author(s):  
Maria Ida Maiorino ◽  
Giuseppe Bellastella ◽  
Michela Petrizzo ◽  
Elisabetta Della Volpe ◽  
Rosanna Orlando ◽  
...  

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