Department of Clinical Laboratory, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan Province, China.
Department of Obstetrics and Gynecology, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan Province, China.
J Mol Histol. 2018 Jun;49(3):317-327. doi: 10.1007/s10735-018-9770-7. Epub 2018 Mar 30.
This study aims to elucidate the mechanisms of Wnt/β-catenin signaling pathway in the development of preeclampsia (PE). The mRNA levels of Wnt1, β-catenin, c-myc and cyclinD1 were determined by real-time PCR in the placentas. Moreover, the expression levels of Wnt1, β-catenin, Dickkopf-1 (DKK1) and glycogen synthase kinase 3β (GSK-3β) proteins were detected by Western blot. Immunohistochemistry was used in placental tissue microarray to localize the expression of Wnt1, β-catenin, DKK1 proteins in the placentas of two groups. Compared with the control placentas, the mRNA levels of Wnt1, β-catenin, c-myc and cyclinD1 were decreased in the severe preeclamptic placentas. The Western blot results showed that the expression levels of Wnt1, β-catenin, and GSK-3β proteins were significantly elevated in the control group, while the expression level of DKK1 was significantly decreased. In addition, the staining intensity of Wnt1, β-catenin were weaker in the placentas of the severe PE group while the staining intensity of DKK1 was significantly stronger in the placentas of the severe PE group. Wnt/β-catenin signaling pathway may play a significant role in the pathogenesis of PE by regulating the invasion and proliferation of trophoblast.
本研究旨在阐明 Wnt/β-连环蛋白信号通路在子痫前期(PE)发病机制中的作用。采用实时 PCR 法检测胎盘组织中 Wnt1、β-连环蛋白、c-myc 和 cyclinD1 的 mRNA 水平。同时,采用 Western blot 法检测 Wnt1、β-连环蛋白、Dickkopf-1(DKK1)和糖原合成酶激酶 3β(GSK-3β)蛋白的表达水平。采用免疫组织化学法检测胎盘组织微阵列中两组胎盘组织中 Wnt1、β-连环蛋白、DKK1 蛋白的表达。与对照组胎盘相比,重度子痫前期胎盘中 Wnt1、β-连环蛋白、c-myc 和 cyclinD1 的 mRNA 水平降低。Western blot 结果显示,对照组中 Wnt1、β-连环蛋白和 GSK-3β 蛋白的表达水平显著升高,而 DKK1 的表达水平显著降低。此外,重度 PE 组胎盘中 Wnt1、β-连环蛋白的染色强度较弱,而重度 PE 组胎盘中 DKK1 的染色强度显著增强。Wnt/β-连环蛋白信号通路可能通过调节滋养细胞的侵袭和增殖在 PE 的发病机制中发挥重要作用。