Therapeutics Discovery and Vascular Function in Pregnancy Group, Department of Obstetrics and Gynaecology, University of Melbourne, Victoria, Australia; Translational Obstetrics Group, Department of Obstetrics and Gynaecology, University of Melbourne, Victoria, Australia; Mercy Perinatal, Mercy Hospital for Women, Victoria, Australia.
Translational Obstetrics Group, Department of Obstetrics and Gynaecology, University of Melbourne, Victoria, Australia; Mercy Perinatal, Mercy Hospital for Women, Victoria, Australia.
Placenta. 2020 Jun;95:53-61. doi: 10.1016/j.placenta.2020.04.012. Epub 2020 Apr 26.
Oxidative damage and biochemical ageing are implicated in placental dysfunction and potentially fetal death. Cellular senescence may play a role in the pathophysiology of fetal growth restriction (FGR) and preeclampsia (PE). Aurora kinases (AURKA, B and C) are important regulators of cellular division in mitosis and meiosis with implications in cellular senescence. We aimed to investigate whether aurora kinase expression is altered with placental dysfunction or placental ageing.
Placenta and blood was obtained across gestation from pregnancies complicated by PE, FGR or both PE and FGR, as well as gestation-matched control samples. Expression of AURKA, B and C mRNA was examined using real time qPCR in both the placenta and maternal circulation.
Placental aurora kinase expression decreased as gestation progressed: AURKA and AURKB were significantly reduced at 37-40 weeks, whereas AURKC was significantly reduced at 34-37 weeks, when compared to <34 weeks. In the maternal circulation, the mRNA level of AURKB was significantly reduced at >40 weeks compared to <34 weeks gestation. A significant reduction in AURKC was seen in FGR pregnancies <34 weeks compared to gestation-matched controls.
Placental AURK expression is reduced with increased gestation. Circulating AURKB mRNA reduces at >40 weeks gestation, when compared to <34 weeks. AURKC is significantly reduced in placentas from pregnancies complicated by severe early onset (<34 weeks) FGR compared with gestation-matched controls. The functional role of aurora kinase in the placenta and in gestational age warrants further investigation.
氧化损伤和生化衰老与胎盘功能障碍及胎儿死亡有关。细胞衰老可能在胎儿生长受限（FGR）和子痫前期（PE）的病理生理学中发挥作用。极光激酶（AURKA、B 和 C）是有丝分裂和减数分裂中细胞分裂的重要调节因子，与细胞衰老有关。我们旨在研究胎盘功能障碍或胎盘老化时极光激酶的表达是否发生改变。
从妊娠合并 PE、FGR 或 PE 和 FGR 的妊娠中，以及与妊娠相匹配的对照组中，在整个妊娠期间获得胎盘和血液。使用实时 qPCR 检查胎盘和母血中 AURKA、B 和 C mRNA 的表达。
胎盘极光激酶表达随妊娠进展而降低：与<34 周时相比，AURKA 和 AURKB 在 37-40 周时显著降低，而 AURKC 在 34-37 周时显著降低。在母血中，与<34 周时相比，AURKB mRNA 水平在>40 周时显著降低。与妊娠相匹配的对照组相比，<34 周的 FGR 妊娠中 AURKC 显著减少。
胎盘 AURK 表达随妊娠增加而降低。与<34 周时相比，循环中 AURKB mRNA 在>40 周时减少。与妊娠相匹配的对照组相比，严重早发（<34 周）FGR 妊娠的胎盘中 AURKC 显著减少。极光激酶在胎盘和妊娠年龄中的功能作用值得进一步研究。
