scholarly journals Vascular endothelial function and circulating endothelial progenitor cells in patients with cardiac syndrome X

Heart ◽  
2007 ◽  
Vol 93 (9) ◽  
pp. 1064-1070 ◽  
Author(s):  
P.-H. Huang ◽  
Y.-H. Chen ◽  
Y.-L. Chen ◽  
T.-C. Wu ◽  
J.-W. Chen ◽  
...  
Heart ◽  
2007 ◽  
Vol 93 (9) ◽  
pp. 1071-1076 ◽  
Author(s):  
H. Shmilovich ◽  
V. Deutsch ◽  
A. Roth ◽  
H. Miller ◽  
G. Keren ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Ying Luo ◽  
Zhenhua Huang ◽  
Jinli Liao ◽  
Zhihao Liu ◽  
Xiaopeng Li ◽  
...  

Endothelial progenitor cells (EPCs) have endogenous endothelium-reparative potential, but obesity impairs EPCs. Overweight premenopausal women have a normal number of circulating EPCs with functional activity, but whether EPCs in overweight postmenopausal women can repair obesity-related endothelial damage requires further investigation. For this purpose, we examined the function and number of circulating EPCs, evaluated vascular endothelial function, and explored the underlying mechanism. Compared with normal weight or overweight age-matched men, postmenopausal women (overweight or normal weight) had a diminished number of circulating EPCs and impaired vascular endothelial function, as detected by flow-mediated dilatation. Moreover, GTCPH I expression and the nitric oxide level in overweight postmenopausal women and men were significantly decreased. Together, our findings demonstrate that the number or function of circulating EPCs and endothelial function, which is partially regulated by the GTCPH I/BH4 signaling pathway, is not preserved in overweight postmenopausal women. The GTCPH I/BH4 pathway in circulating EPCs may be a potential therapeutic target for endothelial injury in overweight postmenopausal women.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Ibhar Al Mheid ◽  
Konstantinos Aznaouridis ◽  
Riyaz Patel ◽  
Farheen Shirazi ◽  
Diane J Sutcliffe ◽  
...  

Background: Endothelial Progenitor Cells (EPCs) are mobilized in response to endothelial injury and their counts correlate with endothelial function and cardiovascular risk burden. This rare cell population can be characterized by either flow cytometric analysis or mononuclear cell culture and colony counting, however, the 24-hour circadian variation and inter-relation of EPC measures with endothelial function remain unknown. We hypothesized that EPC levels and endothelial function will have a similar circadian variation. Methods: In 12 healthy subjects (8 men, 42 ± 18 yrs), we investigated the circadian variation of: 1-circulating cells positive for: CD34, CD133 andCD34, the number of colonies formed by culturing mononuclear cells utilizing a 7-day assay and flow-mediated vasodilation utilizing brachial artery reactivity at 8am, noon, 4pm, 8pm, midnight, 4am and 8am. Results: ANOVA for repeated measures over 24 hours indicated significant changes in the number of colony counts (p < .001, highest at midnight). Similarly, flow-mediated vasodilation was highest at midnight (p < .001). In contrast, CD34+ and dual positive CD34+ /CD133+ cell counts peaked a little earlier at 8 pm (8 pm vs.8 am p = .07 and .01 for paired t-tests, respectively). (Figure ) Conclusion: Endothelial function and EPCs estimated as colony forming units peak at midnight and are lower at other times of the day. The highest counts of circulating progenitors are seen at 8pm. There is a parallel change in circulating EPCs and vascular endothelial function during a 24-hour period, with lower levels in the morning hours.


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