胎盘滋养细胞功能失调是导致PE发生的核心环节，VD可通过调节滋养细胞功能进而影响PE的发生。我们已证实VD可特异性上调内皮细胞miR126表达并抑制内皮细胞炎症反应，前期工作发现PE胎盘miR126表达下降，VD可增加滋养细胞miR126表达。生物信息学分析发现COX2和PIK3R2是miR126的靶基因，且初步实验结果显示miR126能抑制滋养细胞COX2表达。胎盘COX2-TXA2:PGI2轴和PIK3R2-PI3K/Akt-sFlt1:PGF轴在PE病理改变中发挥重要作用。因此我们推测VD通过VDR增加滋养细胞miR126表达，引起以下作用：抑制靶分子COX2，降低TXA2:PGI2比率；抑制靶分子PIK3R2，促使PI3K/Akt通路活性增加，降低sFlt1:PGF比率。综上，抑制炎症、促进血管生成并降低血管紧张性。本研究为揭示VD防治PE发生的作用机制提供新的视角。

Dysfunction of placental trophoblast plays a key role in the pathological process of preeclampsia (PE). Vitamin D (VD) can affect the occurrence of PE through regulating trophoblast functions. We have reported that VD could specifically increase miR126 expression and thus inhibit inflammatory response in endothelial cells. Moreover, we found that placental miR126 expression was decreased in preeclampsia, and VD could upregulate miR126 expression in placental trophoblast. Bioinformatics analysis showed that COX2 and PIK3R2 were the target genes of miR126, and our preliminary results showed that miR126 could attenuate COX2 expression in placental trophoblast. Placental COX2-TXA2:PGI2 axis and PIK3R2-PI3K/Akt-sFlt1:PGF axis play an important role in the pathological changes of PE. We therefore hypothesis that VD increases the expression of trophoblast miR126 through VDR, and then cause the following effects: inhibit its target molecule COX2 and lead to TXA2:PGI2 ratio decreased; inhibit its target molecule PIK3R2 and lead to PI3K/Akt pathway activity increased, thus decrease sFlt1:PGF ratio. In summary, placental VD-miR126 attenuates inflammation and vasoconstriction, but promotes angiogenesis in PE. This study provides a theoretical basis and a new perspective to reveal the mechanism of VD prevention of PE.