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Preeclampsia associated changes in volume density of fetoplacental vessels in Chinese women and mouse model of preeclampsia

子痫前期 川地31 下调和上调 免疫组织化学 胎盘 血管造影 血管生成 医学 黑森矩阵 发病机制 螺旋动脉 男科 病理 胎儿 生物 内科学 怀孕 基因 生物化学 遗传学 数学 应用数学
作者
Xinyang Shen,Changjian Wang,Xiaojing Yue,Qianjing Wang,Lijia Xie,Zhenqin Huang,Xiaowei Huang,Jiaqi Li,Yao Xu,Lu Chen,Stephen J. Lye,Zhijian Wang,Zhijian Wang
出处
期刊:Placenta [Elsevier BV]
卷期号:121: 116-125 被引量:3
标识
DOI:10.1016/j.placenta.2022.03.002
摘要

Preeclampsia (PE) is associated with abnormal placental vascular structure. However, the volume density of fetoplacental vessels in PE remains unclear. Additionally, manually annotated CT angiography, which is widely used to analyze placental vessels, has issues regarding inaccuracy. Thus, computer-aided CT angiography for analyzing the volume density of fetoplacental vessels would facilitate the understanding of PE pathogenesis.We performed computer-aided CT angiography to compare differences in placentas among 17 women with PE and 34 normotensive women. The contrast ratio in CT angiography was significantly enhanced using a three-dimensional (3-D) Hessian matrix algorithm. The PE-like mouse model was established by administration of 125 mg/kg/day NG-nitro-l-arginine methyl ester (l-NAME) for 10 days. The presence of endothelial marker CD31 was confirmed by quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry (IHC). The expression of angiogenic factors (PlGF, VEGFA, and sFlt1) in placentas was detected using qRT-PCR and western blotting.The volume density in fetoplacental vessels and CD31 expression were significantly reduced in women with PE and l-NAME-induced mice. Additionally, the downregulation of angiogenic factors (PlGF/VEGFA) and upregulation of an anti-angiogenic factor (sFlt1) were determined in a mouse model.Contrast-enhanced CT angiography with the aid of a 3-D Hessian matrix algorithm was performed. PE significantly affects the formation of vascular vessels, resulting in a lower volume density of fetoplacental vessels in humans and mice. This may be explained by the abnormal release of angiogenic factors during PE.
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