scholarly journals Quantitative and functional characteristics of endothelial progenitor cells in newly diagnosed hypertensive patients

2014 ◽  
Vol 29 (5) ◽  
pp. 324-330 ◽  
Author(s):  
M Skrzypkowska ◽  
J Myśliwska ◽  
B Słomiński ◽  
J Siebert ◽  
P Gutknecht ◽  
...  
2010 ◽  
Vol 4 (4) ◽  
pp. 164
Author(s):  
L. Ryliskyte ◽  
A. Laucevicius ◽  
R. Malickaite ◽  
K. Ryliskiene ◽  
L. Jurgauskiene ◽  
...  

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Jianwen Liang ◽  
Yan Li ◽  
Long Chen ◽  
Wenhao Xia ◽  
Guifu Wu ◽  
...  

Abstract Background Hypertension often presents with microvascular rarefaction (MVR), which is closely associated with impaired angiogenesis. Early detection of MVR is essential for systemic assessment in patient with hypertension. We aimed to determine the systemic MVR through both optical coherence tomography angiography (OCTA) and intravital capillaroscopy, and to investigate their respective efficacies and related mechanisms associated with late endothelial progenitor cells (LEPCs) dysfunction. Methods Seventy-one hypertensive and sixty-nine age-match normotensive subjects were included in this study. All subjects received intravital capillaroscopy for skin capillary density (SCD) and OCTA for retinal capillary density (RCD) and non-perfused areas (R-NPA). Subsequently, correlation of LEPCs activities and microvascular rarefaction were examined. Results Compared with normotensive subjects, hypertensive patients had significantly lower RCD [(52.9 ± 2.9)% vs. (57.8 ± 1.6)%, P < 0.01] and higher R-NPA [(0.12 ± 0.07) mm2 vs. (0.053 ± 0.020) mm2, P < 0.01]. SCD correlated positively with RCD but negatively with R-NPA [(RCD: OR = 0.40, 95% CI 0.25–0.67, P < 0.01); (R-NPA: OR = 0.39, 95% CI − 0.0029 to 0.0011, P < 0.01)]. The discriminative powers of RCD performed best (AUC 0.79 versus SCD AUC 0.59, P < 0.001) followed by R-NPA (AUC 0.73 versus SCD AUC 0.59, P < 0.001) for systolic blood pressure. Similar pattern is also found for diastolic blood pressure (RCD AUC 0.80 versus SCD AUC 0.54, P < 0.001; R-NPA AUC 0.77 versus SCD AUC 0.54, P < 0.001). Furthermore, LEPCs tube formation was impaired in hypertensive patients (36.8 ± 2.3 vs. 28 ± 3.7, P < 0.01). After multivariate adjustments, positive correlation existed between RCD or R-NPA with LEPCs tube formation (RCD: β = 0.64, 95% CI 0.34–0.91, P < 0.01; R-NPA: β = − 24.67, 95% CI − 43.14 to − 4.63, P < 0.05) but not with SCD (β = 0.082, 95% CI 0.01–0.18, P = 0.085). Conclusion Compared to intravital capillaroscopy, OCTA is a more precise technique for early detection of hypertensive microvascular rarefaction, which is associated with the fall in LEPC-mediated angiogenesis. Both of OCTA and LEPCs function can help identify hypertension-related capillary abnormality. Trail Registration The trial is a substudy of EXCAVATION-CHN1, registered at clinicaltrials.gov as NCT02817204 (June 26, 2016).


2014 ◽  
Vol 16 (4) ◽  
pp. 295-300 ◽  
Author(s):  
Maria E. Marketou ◽  
Athanasia Kalyva ◽  
Fragiskos I. Parthenakis ◽  
Charalampos Pontikoglou ◽  
Spyros Maragkoudakis ◽  
...  

Author(s):  
Qingsong Hu ◽  
Yiqun Guo ◽  
Tao Zhang ◽  
Jianyi Feng ◽  
Jinlong Wang ◽  
...  

Dysfunction of late endothelial progenitor cells (EPCs) has been suggested to be associated with hypertension. β2 adrenergic receptor (β2AR) is a novel and key target for EPCs homing. Here, we proposed that attenuated β2AR signaling contributes to EPCs dysfunction, whereas enhanced β2AR signaling restores EPCs' functions in hypertension. EPCs derived from hypertensive patients exhibited reduced cell number, impaired in vitro migratory and adhesion abilities, and impaired re-endothelialization after transplantation in nude mice with carotid artery injury. β2AR expression of EPCs from hypertensive patients was markedly downregulated, whereas the phosphorylation of the p38 mitogen-activated protein kinase (p38-MAPK) was elevated. The cleaved caspase-3 levels were elevated in EPCs. The overexpression of β2AR in EPCs from hypertensive patients inhibited p38-MAPK signaling while enhanced in vitro EPC proliferation, migration and adhesion, and in vivo re-endothelialization. The β2AR-mediated effects were attenuated by treating the EPCs with a neutralizing monoclonal antibody against β2AR, which could be partially antagonized by the p38-MAPK inhibitor SB203580. Moreover, shear stress stimulation, a classic non-pharmacological intervention, increased the phosphorylation levels of β2AR and enhanced the in vitro and in vivo functions of EPCs from hypertensive patients. Collectively, the current investigation demonstrated that impaired β2AR/p38MAPK/caspase-3 signaling at least partially reduced the re-endothelialization capacity of EPCs from hypertensive patients. Restoration of β2AR expression and shear stress treatment could improve their endothelial repair capacity by regulating the p38MAPK/caspase-3 signaling pathway. The clinical significance of β2AR in endothelium repair still requires further investigation.


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