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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。
Objective: To investigate the expression of G-protein coupled receptor 30 (GPR30) on gestational trophoblastic cells and its relationship with the development of preeclampsia (PE) . Methods: The expression of GPR30 in the first trimester of pregnancy was detected by immunofluorescence and immunohistochemistry. The expression of GPR30 in normal pregnancy and PE was detected by immunohistochemistry and Western blot. Human chorionic trophoblast cell line HTR8 / SVneo was treated with hypoxia reoxygenation (H / R) to establish a PE model to detect the expression of GPR30. HTR8 / SVneo cells and villous explants were treated with 17β-estradiol (E2), GPR30-specific agonist G1 and blocker G15 to observe the effect of treatment factors on trophoblast invasiveness. Results: GPR30 was highly expressed in early villus trophoblast cells. GPR30 expression in normal placental trophoblast in late pregnancy was significantly higher than that in PE placenta. GPR30 expression was significantly reduced in the PE cell model. E2 and G1 can increase the ability of trophoblast invasion, G15 can down-regulate its invasiveness. Conclusion: Decreased expression of GPR30 may down-regulate the invasiveness of trophoblast, which may be related to the pathogenesis of PE.