Testosterone Deficiency and Endothelial Dysfunction: Nitric Oxide, Asymmetric Dimethylarginine, and Endothelial Progenitor Cells

2019 ◽  
Vol 7 (4) ◽  
pp. 661-668 ◽  
Author(s):  
Yuji Hotta ◽  
Tomoya Kataoka ◽  
Kazunori Kimura
Keyword(s):  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Asymmetric Dimethylarginine ◽  
Testosterone Deficiency ◽  
Endothelial Progenitor

Widespread endotheliopathy in adults with cyanotic congenital heart disease

2014 ◽  
Vol 25 (3) ◽  
pp. 511-519 ◽  
Author(s):  
Rachael L. Cordina ◽  
Shirley Nakhla ◽  
Shamus O’Meagher ◽  
John Leaney ◽  
Stuart Graham ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Congenital Heart Disease ◽  
Heart Disease ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Congenital Heart ◽  
Asymmetric Dimethylarginine ◽  
Cyanotic Congenital Heart Disease ◽  
Endothelial Progenitor ◽  
Flow Mediated Dilatation

AbstractIntroduction: Cyanotic congenital heart disease is associated with functional limitation and vascular events. The nature and extent of endothelial dysfunction in cyanotic adults is poorly understood. We sought to characterise endothelial function in this setting. Methods: A total of fourteen adults with cyanotic congenital heart disease (40±3 years) together with age- and sex-matched healthy controls underwent assessment of nitric oxide-dependent vascular responses, including flow-mediated dilatation of the brachial artery and dynamic vessel analysis of the retina in response to flickering light. Plasma levels of the endothelium-derived vasoconstrictor endothelin-1 and the nitric oxide antagonist, asymmetric dimethylarginine, were measured. Circulating endothelial progenitor cells were assessed by flow cytometry. Results: Flow-mediated dilatation was significantly lower in cyanosed adults than controls (4.0±0.8 versus 7.2±1.0%, p=0.019, n=11 per group). Retinal arterial and venous dilatory responses were also impaired (2.9±0.8 versus 5.0±0.6%, p=0.05 and 3.4±0.3 versus 5.2±0.7%, p=0.04, n=13). Serum levels of endothelin-1 and asymmetric dimethylarginine were higher in cyanosed adults (3.0±0.6 versus 1.1±0.1 pg/ml, p=0.004 and 0.68±0.05 versus 0.52±0.02 μmol/L, p=0.03, n=11). Endothelial progenitor cells (CD34+CD45dimCD133+KDR+) were reduced in those with chronic cyanosis (17±4 versus 40±6 per million white blood cells, p=0.005, n=11). Conclusions: Endothelial function is impaired in the systemic arteries and retinal vessels in adults with cyanotic congenital heart disease, suggesting a widespread endotheliopathy. Diminished numbers of endothelial progenitor cells might potentially contribute to these observations.

Endothelial Progenitor Cells and Asymmetric Dimethylarginine After Renal Transplantation

2015 ◽  
Vol 25 (2) ◽  
pp. 247-249 ◽  
Author(s):  
Vladimír Teplan ◽  
Andrea Mahrová ◽  
Ivana Králová-Lesná ◽  
Jaroslav Racek ◽  
Ivo Valkovský ◽  
...  
Keyword(s):  
Renal Transplantation ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Asymmetric Dimethylarginine ◽  
Endothelial Progenitor

scholarly journals Asymmetric Dimethylarginine and Endothelial Progenitor Cells After Renal Transplantation: the Effect of Exercise Training

2014 ◽  
pp. S411-S417
Author(s):  
V. TEPLAN ◽  
I. KRÁLOVÁ LESNÁ ◽  
J. PIŤHA ◽  
A. MAHROVÁ ◽  
J. RACEK ◽  
...  
Keyword(s):  
Renal Transplantation ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Asymmetric Dimethylarginine ◽  
Exercise Program ◽  
Cardiovascular Complications ◽  
Hla Typing ◽  
Endothelial Progenitor ◽  
Group I ◽  
Group Ii

Level of asymmetric dimethylarginine (ADMA) is elevated and endothelial progenitor cells (EPC) and stem cells (SC) are decreased in patients undergoing renal transplantation (Tx) and may contribute to cardiovascular complications. We tested the hypothesis that ADMA, EPC and SC can be influenced with regular physical exercise early after Tx. Blood samples of ADMA, EPC, SC, adipocytokines and metabolic parameters were randomly obtained from 50 transplant patients before and 6 months after exercise program (Group I). Fifty age, sex, HLA typing, duration of dialysis and immunosupression regimen-matched non exercising transplant were examined as controls (Group II). After 6 months, in Group I ADMA decreased (3.50±0.45 vs 2.11±0.35 μmol/l, P<0.01) and was lower comparing to Group II (P<0.01), SC and EPC also decreased (2816±600 vs 2071±480 cells/ml resp. 194±87 to 125±67 cells/ml, P<0.02). Next changes in Group I: adiponectin (P<0.01), leptin (P<0.01), resistin (P<0.02). Visfatin, blood lipids, HbA1c, insulin and blood pressure were also influenced by training program (P<0.05).

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.

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