Immunohistochemical expression of von Willebrand factor in the preeclamptic placenta

Immunohistochemical expression of von Willebrand factor in the preeclamptic placenta
复制标题

DOI:
10.1007/s10735-011-9351-5
复制
发表时间:
2011-10-01
影响因子:
3.2
通讯作者:
Rodrigo, Ramon
Rodrigo, Ramon
中科院分区:
生物学4区
文献类型:
--
作者:
Parra-Cordero, Mauro;Bosco, Cleofina;Rodrigo, Ramon

文献摘要

被引文献

相似文献

先兆子痫是一种高患病率的系统性妊娠疾病,与孕产妇和胎儿死亡率相关。其发病机制尚不清楚,但认为氧化应激和内皮功能障碍可能起着重要作用。血管性血友病因子(vWF)是内皮细胞损伤的标志物,可在胎盘的不同细胞和区域中发现。探讨vWF在不同组织类型子痫前期胎盘组织中的表达差异及子痫前期孕妇血清中内皮功能障碍标志物的表达。对先兆子痫孕妇(n = 14)和正常妊娠妇女(n = 8)进行病例对照研究。分娩时抽取胎盘和血浆样本。用免疫组化法检测胎盘组织vWF表达。通过母血中纤溶酶原激活物抑制物(派)1和2比值和vWF浓度评估内皮功能障碍。P值小于0.05被认为具有统计学显著性。子痫前期患者血浆派-1/派-2比值升高(P < 0.05)。子痫前期胎盘合体滋养细胞vWF表达减弱,绒毛间隙vWF表达增强(P < 0.05)。vWF在绒毛内皮和间质中的表达差异无统计学意义,但在母体血浆中的表达明显高于对照组(P < 0.05)。在先兆子痫中发生内皮损伤和胎盘细胞损伤。子痫前期患者合体滋养层细胞的损伤可使vWF从合体滋养层释放到胎盘绒毛间隙,这可能具有致病性。
Preeclampsia is a high-prevalence systemic pregnancy disorder associated with maternal and foetal mortality. Its pathogenesis is unknown, but it is thought that oxidative stress and endothelial dysfunction may play a fundamental role. Von Willebrand factor (vWF), a marker of endothelial cell injury, can be found in different cells and zones of the placenta. To determine the differential immunoexpression of vWF at different tissue types of preeclamptic placenta and endothelial dysfunction markers at maternal serum of preeclamptic pregnancies. A case-control study was performed on a population of pregnant women with preeclampsia (n = 14), and normal pregnancies (n = 8). Placental and blood plasma samples were withdrawn at delivery. Immunohistochemical vWF expression in the placental tissue was determined. Endothelial dysfunction was assessed through plasminogen activator inhibitor (PAI) 1 and 2 ratio and vWF concentration in maternal plasma. P values less than 0.05 were considered statistically significant. Preeclamptic women showed increased plasma PAI-1/PAI-2 ratio (P < 0.05). There was diminished placental vWF expression in syncytiotrophoblast and increased in the intervillous space of preeclamptic placentas (P < 0.05). No significant differences in vWF expression were found in the villous endothelium and stroma, but it was significantly higher in maternal plasma (P < 0.05). In preeclampsia occurs endothelial damage and placental cell injury. Cell damage in syncytiotrophoblast that occurs in preeclampsia could liberate vWF from syncytiotrophoblast to the placental intervillous space, and this may have pathogenic implications.