Shen Xinyang, Wang Changjian, Yue Xiaojing, Wang Qianjing, Xie Lijia, Huang Zhenqin, Huang Xiaowei, Li Jiaqi, Xu Yao, Chen Lu, Lye Stephen, Wei Yanxing, Wang Zhijian
Department of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, 510515, China.
School of Computer, National University of Defense Technology, Changsha, Hunan, 410000, China.
Placenta. 2022 Apr;121:116-125. doi: 10.1016/j.placenta.2022.03.002. Epub 2022 Mar 9.
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.
子痫前期(PE)与胎盘血管结构异常有关。然而,PE患者中胎儿胎盘血管的体积密度仍不清楚。此外,广泛用于分析胎盘血管的手动标注CT血管造影存在不准确的问题。因此,用于分析胎儿胎盘血管体积密度的计算机辅助CT血管造影将有助于理解PE的发病机制。
我们进行了计算机辅助CT血管造影,以比较17例PE患者和34例血压正常女性的胎盘差异。使用三维(3-D)黑塞矩阵算法显著增强了CT血管造影中的对比率。通过给予125mg/kg/天的NG-硝基-L-精氨酸甲酯(L-NAME)10天建立PE样小鼠模型。通过定量实时聚合酶链反应(qRT-PCR)和免疫组织化学(IHC)确认内皮标志物CD31的存在。使用qRT-PCR和蛋白质印迹法检测胎盘中血管生成因子(PlGF、VEGFA和sFlt1)的表达。
PE患者和L-NAME诱导的小鼠中胎儿胎盘血管的体积密度和CD31表达显著降低。此外,在小鼠模型中确定了血管生成因子(PlGF/VEGFA)的下调和抗血管生成因子(sFlt1)的上调。
借助3-D黑塞矩阵算法进行了对比增强CT血管造影。PE显著影响血管的形成,导致人和小鼠中胎儿胎盘血管的体积密度降低。这可能是由于PE期间血管生成因子的异常释放所致。