G-protein-coupled receptor 30 mediates the effects of estrogen on endothelial cell tube formation in vitro.pdf (753.02 kB)
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G-protein-coupled receptor 30 mediates the effects of estrogen on endothelial cell tube formation in vitro

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journal contribution
posted on 30.04.2018, 13:21 by L. Zhou, H. Chen, X. Mao, H. Qi, Philip N. Baker, H. Zhang
The placenta is the exchange organ between the mother and the fetus. The inadequate function of this organ is associated with a number of pregnancy disorders. Hypoxia and oxidative stress during placental development may induce endothelial dysfunction, resulting in the reduction in the perfusion of the placenta. During pregnancy, the levels of estrogen are increased. Decreased estrogen levels have been reported in women with preeclampsia. However, whether estrogen is involved in placental angiogenesis remains unclear. In this study, we aimed to investigate the effects of estrogen on endothelial cell tube formation and to elucidate the underlying mechanisms. For this purpose, human umbilical vein endothelial cells (HUVECs) were cultured with 17‑β‑estradiol under conditions of hypoxia/reoxygenation (H/R). The total pipe length of the tube‑like structure on endothelial cells was measured. The expression levels of G‑protein‑coupled receptor 30 (GPR30) and endothelial nitric oxide synthase (eNOS) and Akt were also measured in the endothelial cells following treatment with 17‑β‑estradiol under H/R conditions by western blot analysis and immunostaining. We found that the total pipe length of the tube‑like structure on endothelial cells was significantly reduced. This reduction was reversed by treatment with 17‑β‑estradiol. The expression of GPR30 in endothelial cells was significantly increased following treatment with 17‑β‑estradiol under H/R conditions. Furthermore, the levels of eNOS and Akt in endothelial cells were also significantly increased following treatment with 17-β-estradiol under H/R conditions. The activation of eNOS was inhibited by wortmannin, an inhibitor of PI3K/Akt. Our data thus demonstrate that estrogen prevents the failure of endothelial cell tube formation induced by H/R. GPR30 plays an important role in these protective effects through the activation of eNOS and Akt in endothelial cells. Our data suggest that increased levels of estrogen are important for placental angiogenesis.

History

Citation

International Journal of Molecular Medicine, 2017, 39 (6), pp. 1461-1467

Author affiliation

/Organisation/COLLEGE OF LIFE SCIENCES

Version

VoR (Version of Record)

Published in

International Journal of Molecular Medicine

Publisher

Spandidos Publications

issn

1107-3756

eissn

1791-244X

Acceptance date

04/04/2017

Copyright date

2017

Available date

30/04/2018

Publisher version

https://www.spandidos-publications.com/10.3892/ijmm.2017.2957

Language

en