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Abstract：
Background and Objectives: Preeclampsia has been linked to an inflammatory response that may be brought on by endothelial cell dysfunction. This paper investigates the pathomechanism of syncytiotrophoblast basement membrane (STBM) damage and Placental Protein 13 (PP13) release, which may have a role in systemic endothelial dysfunction in preeclampsia. Materials and Methods: This comparative cross-sectional study involves 54 preeclampsia patients (27 early-onset preeclampsia and 27 late-onset preeclampsia) and 27 pregnant women with normal blood pressure. An enzyme-linked immunosorbent assay was performed to evaluate maternal blood levels of PP13. Following birth, a portion of the placenta was collected for transmission electron microscope (TEM) and immunohistochemical (IHC) analysis. The data were analyzed using STATA version 15. Results: PP13 expression in the placental syncytiotrophoblast was significantly lower in the early-onset preeclampsia, compared to late-onset preeclampsia and normotensive pregnancy, group (p < 0.001). In contrast, serum PP13 levels were found to be the highest in the early-onset preeclampsia group, although no significant difference were found in mean maternal serum levels of PP13 between the three groups. The decreased PP13 expression in placental syncytiotrophoblast can be attributed to the greater extent of damage in the STBM in early-onset preeclampsia that leads to the release of a larger amount of PP13 into maternal circulation. The hypothesis aligns with the TEM analysis results. Preeclamptic pregnancies showed placental syncytiotrophoblast aponeurosis, whereas normotensive pregnancies did not. Placental lesions and STBM shedding were found to be more pronounced in early-onset preeclampsia compared to late-onset preeclampsia. Conclusions: PP13 and STBM damage may play a role in systemic endothelial dysfunction in preeclampsia.
摘要：
背景和目的：子痫前期与可能由内皮细胞功能障碍引起的炎症反应有关。本文研究了合胞体滋养层基底膜（STBM）损伤和胎盘蛋白13（PP13）释放的病理机制，这可能在先兆子痫的全身内皮功能障碍中发挥作用。材料和方法：这项比较性横断面研究涉及54例先兆子痫患者（27例早发型先兆子痫和27例晚发型先兆子痫）和27例血压正常的孕妇。进行酶联免疫吸附测定以评估母体血液中PP13的水平。出生后,收集部分胎盘进行透射电镜(TEM)和免疫组织化学(IHC)分析.使用STATA版本15分析数据。结果：早发型子痫前期胎盘合胞体滋养层中PP13的表达明显降低，与晚发型先兆子痫和正常血压妊娠相比，组（p<0.001）。相比之下,发现血清PP13水平在早发型先兆子痫组中最高，尽管三组之间的平均母体血清PP13水平没有显着差异。胎盘合胞体滋养层中PP13表达的降低可归因于早发型先兆子痫中STBM的更大程度的损伤,其导致更大量的PP13释放到母体循环中。该假设与TEM分析结果一致。先兆子痫妊娠显示胎盘合胞体滋养层膜，而血压正常的怀孕没有。与晚发型先兆子痫相比，早发型先兆子痫的胎盘病变和STBM脱落更为明显。结论：PP13和STBM损伤可能在子痫前期的全身内皮功能障碍中起作用。
