The present study was designed to compare the ultrastructure of early endothelial progenitor cells (EPCs) derived from rabbit peripheral blood (PB-EPCs) and bone marrow (BM-EPCs). After the cells had been isolated and cultivated up to passage 3, microphotographs obtained from transmission electron microscope were evaluated from qualitative and quantitative (unbiased stereological approaches) points of view. Our results revealed that both cell populations displayed almost identical ultrastructural characteristics represented by abundant cellular organelles dispersed in the cytoplasm. Moreover, the presence of very occasionally occurring mature endothelial-specific Weibel–Palade bodies (WPBs) confirmed their endothelial lineage origin. The more advanced stage of their differentiation was also demonstrated by the relatively low nucleus/cytoplasm (N/C) ratios (0.41 ± 0.19 in PB-EPCs; 0.37 ± 0.25 in BM-EPCs). Between PB-EPCs and BM-EPCs, no differences in proportions of cells occupied by nucleus (28.13 ± 8.97 versus 25.10 ± 11.48%), mitochondria (3.71 ± 1.33 versus 4.23 ± 1.00%), and lipid droplets (0.65 ± 1.01 versus 0.36 ± 0.40%), as well as in estimations of the organelles surface densities were found. The data provide the first quantitative evaluation of the organelles of interest in PB-EPCs and BM-EPCs, and they can serve as a research framework for understanding cellular function.

Intrauterine growth restriction (IUGR) can induce deleterious changes in the modulatory ability of the vascular endothelium, contributing to an increased risk of developing cardiovascular diseases in the long term. However, the mechanisms involved are not fully understood. Emerging evidence has suggested the potential role of endothelial progenitor cells (EPCs) in vascular health and repair. Therefore, we aimed to evaluate the effects of IUGR on vascular reactivity and EPCs derived from the peripheral blood (PB) and bone marrow (BM) in vitro. Pregnant Wistar rats were fed an ad libitum diet (control group) or 50% of the ad libitum diet (restricted group) throughout gestation. We determined vascular reactivity, nitric oxide (NO) concentration, and endothelial nitric oxide synthase (eNOS) protein expression by evaluating the thoracic aorta of adult male offspring from both groups (aged: 19–20 weeks). Moreover, the amount, functional capacity, and senescence of EPCs were assessed in vitro. Our results indicated that IUGR reduced vasodilation via acetylcholine in aorta rings, decreased NO levels, and increased eNOS phosphorylation at Thr495. The amount of EPCs was similar between both groups; however, IUGR decreased the functional capacity of EPCs from the PB and BM. Furthermore, the senescence process was accelerated in BM-derived EPCs from IUGR rats. In summary, our findings demonstrated the deleterious changes in EPCs from IUGR rats, such as reduced EPC function and accelerated senescence in vitro. These findings may contribute towards elucidating the possible mechanisms involved in endothelial dysfunction induced by fetal programming.

Yang L, Ruan L-M, Ye H-H, Cui H-B, Mu Q-T, Lou Y-R, Ji Y-X, Li W-Z, Sun D-H, Chen X-B. Depression is associated with lower circulating endothelial progenitor cells and increased inflammatory markers.

Objective: To test the hypothesis that depression status in subjects without cardiovascular diseases (CVD) or diabetes is associated with depletion of circulating endothelial progenitor cells (EPCs) and impaired endothelial function.

Method: Thirty depressive persons with the first episode of depression (case group) diagnosed according to Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) and 30 healthy people (control group) were investigated. The depression status was estimated using Hamilton Rating Scale of Depression from which the criteria of depression are determined to be >21 score. EPCs labeled with CD34-ECD, CD133-phycoerythrin and kinase insert domain receptor (KDR)-fluorescein isothiocyanate antibodies were counted by flow cytometry in the peripheral blood of patients and control subjects. Mononuclear cells that were positive for CD34/KDR, CD133/KDR and CD34/CD133/KDR within the lymphocyte population were characterised as different phenotypes of EPCs.

Results: There were no significant differences in baseline clinical characteristics between patients and healthy individuals (all p > 0.05). However, patients with depression had significantly lower levels of circulating CD34+CD133+KDR+ EPCs (132.20 ± 17.27 vs. 225.93 ± 9.88, p = 0.000) and endothelial colony-forming units (26.40 ± 3.79 vs. 36.60 ± 2.88, p = 0.000) than that of healthy subjects. Furthermore, CD34+CD133+KDR+ EPCs had a negative correlation with tumour necrosis factor-α (Spearman's ρ = 0.433, p = 0.000) and interleukin-6 (Spearman's ρ = 0.441, p = 0.032).

Conclusion: Our result shows that depression was associated with lower levels of circulating EPCs, which may contribute to the development of endothelial dysfunction and atherosclerosis.

Juvenile obesity is associated with cardiovascular risk factors. In adults, cardiovascular risk factors and obesity are associated with a decreased number of endothelial progenitor cells. Higher physical fitness correlates with a lower cardiovascular morbidity and increased endothelial progenitor cells.