Kasoha Mariz, Takacs Zoltan, Fackiner Lena, Gerlinger Christoph, Sklavounos Panagiotis, Radosa Julia, Solomayer Erich-Franz, Hamza Amr
Department of Gynecology, Obstetrics and Reproductive Medicine, University Medical School of Saarland, Homburg/Saar, Germany.
Geburtshilfe Frauenheilkd. 2021 Nov 4;81(11):1247-1255. doi: 10.1055/a-1557-1234. eCollection 2021 Nov.
Preeclampsia remains a major cause of perinatal and maternal mortality and morbidity worldwide. Wnt/β-catenin signaling is known to be critically involved in placenta development processes. Dickkopf-1 (DKK1) is a key regulator of this transduction pathway. The aim of this study is to compare maternal serum DKK1 levels and placental mRNA levels of and β-catenin in preeclamptic and normal pregnant women at delivery. The present study included 30 women with preeclampsia and 30 women with normal pregnancy. Maternal serum DKK1 levels were measured by ELISA. Placental mRNA levels of and β-catenin were detected using RT-PCR. Decreased maternal serum DKK1 levels were associated with worse maternal and fetal complications including HELLP syndrome, determination of one or more pathological symptom and IUGR diagnosis. No significant difference in maternal serum DKK1 levels was reported between preeclamptic women and women with normal pregnancy. Placental mRNA levels were lower in preeclamptic women compared with normal pregnant women. Placental mRNA β-catenin levels showed no significant difference between two groups. Our findings reported the aberrant placental mRNA levels in patients with preeclampsia. In addition, worse preeclampsia features were associated with decreased maternal serum DKK1 levels. Hence, aberrant Wnt/β-catenin signaling might present a plausible mechanism in preeclampsia pathogenicity. Dysregulated expression of DKK1 at gene level in the placenta but not at protein level in the maternal serum might confirm the notion that preeclampsia is a type of placenta-derived disease.
子痫前期仍然是全球围产期和孕产妇死亡及发病的主要原因。已知Wnt/β-连环蛋白信号通路在胎盘发育过程中起关键作用。Dickkopf-1(DKK1)是该转导通路的关键调节因子。本研究的目的是比较子痫前期孕妇和正常孕妇分娩时母血DKK1水平以及胎盘mRNA水平和β-连环蛋白水平。本研究纳入了30例子痫前期患者和30例正常孕妇。采用酶联免疫吸附测定法(ELISA)检测母血DKK1水平。使用逆转录聚合酶链反应(RT-PCR)检测胎盘mRNA水平和β-连环蛋白水平。母血DKK1水平降低与包括HELLP综合征、一种或多种病理症状的判定以及胎儿生长受限诊断在内的更严重的母婴并发症相关。子痫前期患者与正常孕妇的母血DKK1水平未见显著差异。子痫前期孕妇的胎盘mRNA水平低于正常孕妇。两组间胎盘mRNAβ-连环蛋白水平未见显著差异。我们的研究结果报道了子痫前期患者胎盘mRNA水平异常。此外,子痫前期更严重的特征与母血DKK1水平降低相关。因此,异常的Wnt/β-连环蛋白信号通路可能是子痫前期发病机制中一个合理的机制。胎盘基因水平上DKK1表达失调而母血蛋白水平未见异常,这可能证实了子痫前期是一种胎盘源性疾病的观点。