Role of NO Pathway in Membrane Estrogen Receptor Mediated Proliferation and Apoptosis of Endothelial Progenitor Cells
- VernacularTitle:膜雌激素受体介导的NO途径对EPCs增殖和凋亡的影响
- Author:
Zhi TAN
;
Yuhong CUI
;
Qiuling XIANG
;
Guiping LIN
;
Tinghuai WANG
- Publication Type:Journal Article
- Keywords:
estrogen;
membrane estrogen receptor;
endothelial progenitor cells;
nitric oxide
- From:
Journal of Sun Yat-sen University(Medical Sciences)
2010;31(1):64-68
- CountryChina
- Language:Chinese
-
Abstract:
[Objective] The aim of the present study was to investigate the role of membrane estrogen receptor (mER) mediated pathway in the proliferation and apoptosis of endothelial progenitor cells (EPCs). [Methods] Bone marrow (BM)-derived EPCs were cultured. The cells were divided into different groups, plus or not plus estrogen receptor blocker (ICI 182,780), PI3K inhibitors (LY294002), and NOS inhibitor (L-NAME) to show the effect of E_2-BSA on EPCs. The proliferation of EPCs was determined by MTT and nitric oxide (NO) release was measured by chromatometry. Apoptotic cell death was determined using the Hochest 33258 staining. The expression of phosphorylated eNOS (p-eNOS) were detected by Western blot. [Results] E_2-BSA could increase EPCs proliferation, and this effect was inhibited by estrogen receptor blocker ICI 182,780, thus indicated that mER-initiated membrane signaling pathways were involved in the action of estrogen on EPCs. E_2-BSA increased nitric oxide production and inhibited apoptosis induced by serum withdrawal, and this effect also inhibited by PI3K inhibitor (LY294002), NOS inhibitor (L-NAME)and estrogen receptor blocker(ICI 182,780), thus indicated that PI3K/Akt/NO pathway was involved the effect of estrogen on EPCs apoptosis. Moreover, E_2-BSA treatment increased phosphorylation of eNOS (p-eNOS). PI3K inhibitors (LY294002) also blocked these effects. [Conclusions] The results of present study suggested that mER mediated EPCs proliferation and apoptosis were related to the PI3K/Akt/eNOS pathway.
