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Endothelial progenitor cells (EPCs) are crucial endogenous endothelium-reparative potentials for endothelial injury, impairments in EPC function may contribute to adiposity-related cardiovascular risk. Obesity is associated with a reversible functional impairment of EPCs, which is primary cardiovascular risk factors. The function of circulating EPCs in obesity overweight premenopausal women is preserved, however, whether this favorable effect still exists in overweight postmenopausal women is not clear. In this study, we aimed to investigate the effect of overweight on function of circulating EPCs and its underlying mechanism.
This study compared the functional activity of circulating EPCs in normal weight or overweight postmenopausal women and normal weight or overweight age-matched men, evaluated the vascular endothelial function in each groups, and investigated the possible underlying mechanism.
We found that compared with normal weight postmenopausal women or age-matched men with or without overweight, the function of circulating EPCs, as well as endothelial function evaluated by flow-mediated dilatation (FMD) in overweight postmenopausal women were lower, which were not preserved. In parallel, the GTCPH I/BH4 signaling pathway and the plasma NO level or NO secretion of circulating EPCs in postmenopausal women was also not retained, in other word, compared in overweight or normal weight men and normal weight postmenopausal women, the phosphorylation of GTCPH I/BH4 signaling pathway and the plasma NO level or NO secretion of circulating EPCs was reduced in overweight postmenopausal women.
The present findings firstly demonstrate that the unfavorable effects of the activity of circulating EPCs in overweight postmenopausal women, which is at least partially related to the decrease of phosphorylation of GTCPH I/BH4 signaling pathway and reduced nitric oxide bioavailability. The GTCPH I/BH4 signaling pathway may be a potential target of therapy for vascular endothelial injury in overweight postmenopausal women.