Abstract
Hyperhomocysteinemia (HHcy) induced endothelial dysfunction is associated with disturbance in circulating endothelial progenitor cells (EPCs). Nevertheless, whether this unfavorable effect of HHcy on circulating EPCs also exists in premenopausal women is still unknown. Therefore, this leaves an area for the investigation of the difference on the number and activity of circulating EPCs in premenopausal women with hyperhomocysteinemia and its underlying mechanism. The number of circulating EPCs was measured by fluorescence-activated cell sorter analysis, as well as DiI-acLDL and lectin fluorescent staining. The migration and proliferation of circulating were evaluated by the Transwell chamber assay and MTT. Additionally, the endothelial function and levels of nitric oxide (NO), VEGF, and GM-CSF in plasma and culture medium were determined. The number or activity of circulating EPCs and flow-mediated dilatation (FMD) in premenopausal women with or without HHcy were higher than those in postmenopausal women. However, no significant effect of HHcy on the number or activity of circulating EPCs in premenopausal women was observed. A similar alteration in NO level between the four groups was observed. There was a correlation between FMD and the number or activity of EPCs, as well as NO level in plasma or secretion by EPCs. For the first time, our findings illuminated the quantitive or qualitative alterations of circulating EPCs and endothelial function in premenopausal patients with HHcy are preserved, which was associated with retained NO production. The recuperated endothelial repair capacity is possibly the potential mechanism interpreting cardiovascular protection in premenopausal women with HHcy.
Highlights
Hyperhomocysteinemia (HHcy) induced endothelial dysfunction, accelerating vascular injury in part as a result of atherosclerosis, is one of the independent risk factors for coronary heart diseases (CHD) and other cardiovascular diseases (CVD) [1,2,3,4,5]
Numerous clinical and epidemiological have demonstrated HHcy was significantly associated with flow-mediated dilatation (FMD) reduction, indicting potential vascular endothelial injury [6]. is injury-induced endothelial dysfunction plays a crucial role in the initiation of atherosclerosis. e nature of endothelial dysfunction represents an imbalance between the magnitude of injury and the repair capacity, increased the peripheral resistance, and further aggravating the endothelial injury, constituted a vicious cycle [5]. erefore, it is critical to accelerate endothelial repair and maintenance vascular endothelial integrity for the prevention and treatment of CVD by HHcy
The FMD in postmenopausal women was lower than premenopausal women. e FMD in the HHcy group was lower than the control group, (P < 0.05), but there was no significant difference in terms of FMD between HHcy premenopausal women and healthy premenopausal women. ere was no significant difference in systolic blood pressure, diastolic blood pressure, HDL, Cr, BUN, LDL, TC, TG, AST, ALT, and FPG for four groups (P > 0.05)
Summary
Hyperhomocysteinemia (HHcy) induced endothelial dysfunction, accelerating vascular injury in part as a result of atherosclerosis, is one of the independent risk factors for coronary heart diseases (CHD) and other cardiovascular diseases (CVD) [1,2,3,4,5]. Erefore, we hypothesize that the number and functional activity of circulating EPCs in HHcy premenopausal women may be different form postmenopausal women with HHcy. In addition, nitric oxide (NO), vascular endothelial growth factor (VEGF), and granulocyte-macrophage colony-stimulating factor (GM-CSF) plays an important role in regulating mobilization, as well as migration and proliferation of circulating EPCs [16,17,18,19]
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