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.

Abstract 3157: Depletion of Circulating Endothelial Progenitor Cells and Endothelial Dysfunction in Subjects with Depressive Symptoms

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Hua Chen ◽  
Jianati Qiuwaxi ◽  
Ching-Yuen Wong ◽  
Sheung-Wai Li ◽  
Hiu-Ting Chan ◽  
...  
Keyword(s):  
Depressive Symptoms ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Multivariate Regression Analysis ◽  
Depression Score ◽  
Endothelial Progenitor ◽  
Circulating Endothelial Progenitor Cells ◽  
Depression Status

Introduction: Although the mechanisms remain unclear, depression is associated with endothelial dysfunction and increases risk of cardiovascular disease (CVD). Recent studies suggest that circulating endothelial progenitor cells (EPC) play an important role in endothelial repair and correlate with endothelial function. Hypothesis: We assessed the hypothesis that the presence of depressive symptoms in subjects without significant CVD is associated with depletion of circulating EPC and impaired endothelial function. Methods: We studied the relationship between the level of circulating EPCs, endothelial function and depression status in 129 healthy normal individuals (54±10 yrs, 54 men) without prior CVD or diabetes. The numbers of circulating CD34/KDR + EPCs were determined by flow cytometry, and the depression status was estimated by Depression Anxiety Stress Scales. Brachial artery flow-mediated dilation (FMD) was measured by high-resolution vascular ultrasound imaging. Results: The median depression score of the study population was 4 (range 0 to 34), and 41 subjects (32 %) had high depression score (DS) ≥8 (defined by ≥ the 75th percentile of the depression score). There were no significant differences in baseline clinical characteristics between subjects with or without high DS (all P > 0.05 ). However, subjects with high DS had significantly lower FMD (5.4±2.7 vs. 8.0±4.0 %, P < 0.001 ) and CD34/KDR + EPC% (1.24±1.27 vs. 2.02±2.43 %, P = 0.037 ) than those with normal DS. Multivariate regression analysis revealed that a high DS (OR 1.08, 95%CI: 1.02–1.15, P = 0.009 ) and old age (OR 1.05, 95%CI: 1.01–1.09, P = 0.029 ) were independent predictors for decreased FMD. Conclusions: The results of this study demonstrated that in subjects without significant CVD, the presence of a high DS was associated with impaired brachial FMD and depletion of circulating EPC. Nevertheless, only depression score, but not the percentage of circulating EPC significantly correlated brachial FMD, and was an independent predictor for impaired brachial FMD.

scholarly journals Rejuvenated Circulating Endothelial Progenitor Cells and Nitric Oxide in Premenopausal Women with Hyperhomocysteinemia

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Long Peng ◽  
Qianlin Gu ◽  
Zhenhua Huang ◽  
Lijin Zeng ◽  
Chang Chu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Function ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Premenopausal Women ◽  
Underlying Mechanism ◽  
No Production ◽  
Endothelial Progenitor ◽  
Repair Capacity ◽  
Circulating Endothelial Progenitor Cells

Hyperhomocysteinemia (HHcy) induced endothelial dysfunction is associated with disturbance in circulating endothelial progenitor cells (EPCs). Nevertheless, whether this unfavorable effect of HHcy on circulating EPCs also exists in premenopausal women is still unknown. Therefore, this leaves an area for the investigation of the difference on the number and activity of circulating EPCs in premenopausal women with hyperhomocysteinemia and its underlying mechanism. The number of circulating EPCs was measured by fluorescence-activated cell sorter analysis, as well as DiI-acLDL and lectin fluorescent staining. The migration and proliferation of circulating were evaluated by the Transwell chamber assay and MTT. Additionally, the endothelial function and levels of nitric oxide (NO), VEGF, and GM-CSF in plasma and culture medium were determined. The number or activity of circulating EPCs and flow-mediated dilatation (FMD) in premenopausal women with or without HHcy were higher than those in postmenopausal women. However, no significant effect of HHcy on the number or activity of circulating EPCs in premenopausal women was observed. A similar alteration in NO level between the four groups was observed. There was a correlation between FMD and the number or activity of EPCs, as well as NO level in plasma or secretion by EPCs. For the first time, our findings illuminated the quantitive or qualitative alterations of circulating EPCs and endothelial function in premenopausal patients with HHcy are preserved, which was associated with retained NO production. The recuperated endothelial repair capacity is possibly the potential mechanism interpreting cardiovascular protection in premenopausal women with HHcy.

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