Effect of GPR30 protein on function of trophoblast cells and its relationship with the development of preeclampsia

Feng Xiang; Zhang Hua

doi:10.13406/j.cnki.cyxb.000840

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Effect of GPR30 protein on function of trophoblast cells and its relationship with the development of preeclampsia

更新时间：2024-01-17

- Effect of GPR30 protein on function of trophoblast cells and its relationship with the development of preeclampsia
- Journal of Chongqing Medical University Vol. 41, Issue 2, Pages: 159-164(2016)
- 作者机构：
  
  重庆医科大学附属第一医院妇产科
- 作者简介：
- 基金信息：
- DOI：10.13406/j.cnki.cyxb.000840
  CLC： R714.244
- Published：2016，
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[1]冯祥,张华.GPR30蛋白对滋养细胞功能的影响与子痫前期发病的关系[J].重庆医科大学学报,2016,41(02):159-164.

Feng Xiang, Zhang Hua. Effect of GPR30 protein on function of trophoblast cells and its relationship with the development of preeclampsia. [J]. Journal of Chongqing Medical University 41(2):159-164(2016)
[1]冯祥,张华.GPR30蛋白对滋养细胞功能的影响与子痫前期发病的关系[J].重庆医科大学学报,2016,41(02):159-164. DOI： 10.13406/j.cnki.cyxb.000840.

Feng Xiang, Zhang Hua. Effect of GPR30 protein on function of trophoblast cells and its relationship with the development of preeclampsia. [J]. Journal of Chongqing Medical University 41(2):159-164(2016) DOI： 10.13406/j.cnki.cyxb.000840.

摘要

目的:探讨G-蛋白偶联受体30（G-protein coupled receptor 30

GPR30）在不同妊娠状态时的滋养细胞上的表达情况

以及其表达变化与子痫前期（preeclampsia

PE）发病的关系。方法:应用免疫荧光及免疫组化的方法检测不同孕周早孕期绒毛中GPR30的表达

应用免疫组化及Western blot检测晚孕期正常和PE患者胎盘组织中GPR30的表达水平。用缺氧复氧（hypoxiareoxygenation

H/R）处理人类绒毛膜滋养层细胞株HTR8/SVneo以建立PE模型

检测其GPR30的表达状况。用17β-雌二醇（17β-estradiol

E2）、GPR30特异性激动剂G1和阻滞剂G15处理HTR8/SVneo细胞及绒毛外植体

观察处理因素对滋养层细胞侵袭力的影响。结果:GPR30在早期绒毛组织细胞滋养细胞上表达水平高;晚孕期正常胎盘滋养细胞上GPR30的表达明显高于PE胎盘。在PE细胞模型上GPR30表达明显减少。E2及G1可增加滋养细胞的侵袭能力

G15则可下调其侵袭力。结论:GPR30表达降低可能下调滋养细胞侵袭力

从而与PE发病有关。

Abstract

Objective:To characterize the expression of G-protein coupled receptor 30(GPR30)in trophoblast cells at different conditions

and to determine the effect of disordered expression of GPR30 on the development of preeclampsia(PE). Methods:The expressions of GPR30 protein were detected not only in villi at first trimester

placentas from normal term and pregnancies complicated with PE

but also in HTR8/SVneo cells which treated with normoxia and hypoxia-reoxygenation(H/R)by immunofluorescence

immunohistochemistry and/or Western blot. The pharmacological modulations of GPR30 were built by the using of 17 β-estradiol(E2)

GPR30 specific agonist G1 and GPR30 specific inhibitor G15. H/R was applied to simulate the pathological condition of PE;their effect on human trophoblast cell invasion was determined using vitro invasion assays. Results:GPR30 protein was highly expressed in the cytotrophoblast of first trimester villi and the term placentas from the gestational matched controls(GMCs)

but significantly compromised in PE cells model and placentas which complicated by PE. In addition

E2 and G1 treatment significantly increased the invasive capacity of trophoblast cells

however

the antagonist G15 play an opposite role. Meanwhile

H/R significantly attenuated invasiveness of trophoblast cells. Conclusion:the pathogenetic mechanism of PE is associated with the downregultaion of GPR30 protein level in trophoblast which may impair the invasive capacity of trophoblast cells.

关键词

G-蛋白偶联受体30子痫前期滋养细胞侵袭力

Keywords

g-protein coupled receptor 30preeclampsiatrophoblast cellsinvasion

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Related Institution

Department of Obstetrics and Gynecology，The First Affiliated Hospital of Chongqing Medical University，Canada-China-New Zealand Joint Laboratory of Maternal and Fetal Medicine of Chongqing Medical University

Department of Medical Genetics and Prenatal Diagnosis，Wuxi Maternal and Child Health Hospital

Department of Obstetrics and Gynecology，Third Affiliated Hospital of Zunyi Medical University， Zunyi First People’s Hospital

Department of Emergency and Intensive Care Unit,The First Affiliated Hospital of Chongqing Medical University

Laboratory of Reproductive Biology,School of Public Health and Management,Chongqing Medical University,Canada-China-New Zealand Joint Laboratory of Maternal and Fetal Medicine of Chongqing Medical University

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