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Title: G protein-coupled receptor 30 regulates trophoblast invasion and its deficiency is associated with preeclampsia
Authors: Tong, Chao
Feng, Xiang
Chen, Jun
Qi, Xingchen
Zhou, Liyuan
Shi, Shuming
Kc, Kamana
Stanley, Joanna L.
Baker, Philip N.
Zhang, Hua
First Published: 1-Apr-2016
Publisher: Wolters Kluwer Health, Inc.
Citation: Journal of Hypertension, 2016, 34 (4), pp. 710-718
Abstract: BACKGROUND: Preeclampsia is known to be associated with reduced circulating levels of estrogen. The effects of estrogen in preeclampsia are normally mediated by the classical estrogen receptors. Intriguingly, a novel estrogen receptor, G protein-coupled receptor 30 (GPR30), has been recently found to play an important role in several estrogenic effects. However, the mechanisms by which GPR30 may mediate the development of preeclampsia remain unknown. METHOD: We observed that the expression of GPR30 in placental trophoblast cells is lower in preeclamptic placentas compared with normotensive controls. We then investigated the role of GPR30 in trophoblast cell invasion by utilizing placental explants and the immortalized human trophoblast cell line (HTR8/SVneo). RESULTS: The selective GPR30 agonist G1 and a general estrogen receptors agonist 17-β-estradiol (E2) both improved trophoblast cells invasion by upregulating MMP9 expression and the PI3K-Akt signaling pathway. This effect was abolished by a selective GPR30 inhibitor G15, implying that GPR30 may be involved in regulating trophoblast invasion, and that down-regulation of this receptor may result in the development of preeclampsia. CONCLUSION: The present study suggests that GPR30 is a critical regulator of trophoblast cell invasion, and as such may be a potential therapeutic interventional target for preeclampsia and other pregnancy complications resulting from impaired trophoblast invasion.
DOI Link: 10.1097/HJH.0000000000000844
ISSN: 0263-6352
eISSN: 1473-5598
Version: Post-print
Status: Peer-reviewed
Type: Journal Article
Rights: Copyright © Wolters Kluwer Health, Inc., 2016. This version of the article is distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License ( ), which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
Description: Following the embargo period the above license applies.
Appears in Collections:Published Articles, College of Medicine, Biological Sciences and Psychology

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