Downregulated GTCPH I/BH4 Pathway and Decreased Function of Circulating Endothelial Progenitor Cells and Their Relationship with Endothelial Dysfunction in Overweight Postmenopausal Women

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...

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Bibliographic Details
Published in:Stem cells international 2018-01, Vol.2018 (2018), p.1-11
Main Authors: Zeng, Haitao, Yan, Quanneng, Zhan, Hong, Hu, Da-Jun, He, Hao, Yao, Shun, Li, Xiao-Peng, Liu, Zhihao, Liao, Jinli, Huang, Zhenhua, Luo, Ying, Ren, Zi
Format: Article
Language:English
Subjects:
Body weight
Cardiovascular disease
Cells (biology)
Comparative analysis
Endothelium
Health risk assessment
Low density lipoprotein
Menopause
Nitric oxide
Obesity
Overweight
Post-menopause
Postmenopausal women
Progenitor cells
Sapropterin dihydrochloride
Signal transduction
Stem cells
Stretching
Therapeutic applications
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Summary: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.
ISSN:1687-966X
1687-9678
1687-9678
DOI:10.1155/2018/4756263