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Imbalance between proliferation and apoptosis-related impaired GPR30 expression is involved in preeclampsia.

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journal contribution
posted on 03.01.2017, 15:45 by J. Li, Z. Chen, X. Zhou, S. Shi, H. Qi, Philip N. Baker, H. Zhang
The proliferation and apoptosis of cells in the placenta play a critical role in preeclampsia (PE) in which estrogen has been implicated via estrogen receptors (ERs). A novel ER, G-protein-coupled receptor 30 (GPR30), has recently been shown to be involved in PE. We investigated the basic levels of proliferation and apoptosis in normal placentae and placentae with PE and compared GPR30 expression levels between the two groups. We demonstrated that low GPR30 expression levels, more apoptosis, and less proliferation were associated with PE. Moreover, our in vitro study showed that both the selective GPR30 agonist G1 and the general ER agonist 17-β-estradiol were able to protect the placenta from hypoxia-reoxygenation injuries, resulting in decreased apoptosis and increased proliferation. Furthermore, this protective effect was abolished by the addition of the selective GPR30 inhibitor G15. These results provide evidence that (1) GPR30 is involved in regulating cell proliferation and apoptosis; (2) pharmacologic upregulation of GPR30 is beneficial for PE management; (3) GPR30 may therefore be an interventional target for pregnancies complicated by PE.

Funding

This study was financially supported by the National Natural Science Foundation of China (grant nos. 81370732 and 81571453).

History

Citation

Cell and Tissue Research, 2016, 366 (2), pp. 499-508

Author affiliation

/Organisation/COLLEGE OF MEDICINE, BIOLOGICAL SCIENCES AND PSYCHOLOGY

Version

AM (Accepted Manuscript)

Published in

Cell and Tissue Research

Publisher

Springer Verlag (Germany)

issn

0302-766X

eissn

1432-0878

Available date

01/08/2017

Publisher version

http://link.springer.com/article/10.1007/s00441-016-2466-y

Language

en

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