Coulter Department of Biomedical Engineering, Emory University and Georgia Institute of Technology, Atlanta, GA, 30322, USA.
Division of Cardiology, Department of Medicine, Emory University School of Medicine, 101 Woodruff Circle, Woodruff Memorial Building (WMB) 3309, Atlanta, GA, 30322, USA.
Sci Rep. 2021 Feb 11;11(1):3630. doi: 10.1038/s41598-021-83146-8.
Preeclampsia (PE) is a prevalent pregnancy disorder that leads to high maternal and fetal morbidity and mortality. While defective vascular development and angiogenesis in placenta are known as crucial pathological findings, its pathophysiological mechanism remains elusive. To better understand the effects of PE on angio-vasculogenesis and inflammatory networks in the fetus and to identify their biological signatures, we investigated the quantitative and functional characteristics of cord blood-derived mononuclear cells (CB-MNCs) and CD31-positive MNCs. Flow cytometry analysis demonstrated that the CB-MNCs from the severe PE group had significantly decreased number of cells expressing CD3, CD11b, CD14, CD19, KDR, and CD31 compared with the normal group. Quantitative real time PCR (qRT-PCR) shows down-regulation of the major angiogenic factor VEGFA in MNCs and CD31 MNCs in severe PE. The major inflammatory cytokines IL1 was highly upregulated in CD31 CB-MNCs in the severe PE patients. Mild PE patients, however, did not display any significant difference in expression of all measured angiogenic genes and most inflammatory genes. These findings show distinct angiogenic and inflammatory signatures from severe PE, and they may play a significant role in the pathogenesis of vascular defects in placenta of severe PE.
子痫前期（PE）是一种常见的妊娠疾病，可导致孕产妇和胎儿发病率和死亡率升高。尽管已知胎盘血管发育和血管生成缺陷是关键的病理发现，但其病理生理机制仍不清楚。为了更好地了解 PE 对胎儿血管生成和炎症网络的影响，并确定其生物学特征，我们研究了脐带血衍生的单核细胞（CB-MNCs）和 CD31 阳性 MNCs 的定量和功能特征。流式细胞术分析表明，与正常组相比，严重 PE 组的 CB-MNCs 表达 CD3、CD11b、CD14、CD19、KDR 和 CD31 的细胞数量显著减少。定量实时 PCR（qRT-PCR）显示，MNCs 和 CD31 MNCs 中主要血管生成因子 VEGFA 的表达下调。严重 PE 患者的 CD31 CB-MNCs 中主要炎症细胞因子 IL1 高度上调。然而，轻度 PE 患者在所有测量的血管生成基因和大多数炎症基因的表达中均未显示出任何显著差异。这些发现表明严重 PE 存在明显的血管生成和炎症特征，它们可能在严重 PE 胎盘血管缺陷的发病机制中发挥重要作用。
