Cyclophilin A inhibits trophoblast migration and invasion in vitro and vivo through p38/ERK/JNK pathways and causes features of preeclampsia in mice

环丝氨酸蛋白酶 A 通过 p38/ERK/JNK 通路抑制滋养细胞体外和体内迁移和侵袭,并导致小鼠出现先兆子痫的特征

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作者:Haoyue Hu, Jiayi Jiang, Qian Chen, Songren Wei, Mian Liu, Xia Chen, Cuixia Fan, Jing Ma, Wenqian Chen, Xuefei Wang, Mei Zhong

Aims

Numerous studies suggest that excessive maternal inflammation and defective extravillous trophoblast (EVT) invasion could contribute to the development of preeclampsia (PE), but the underlying mechanism remains unclear. Some evidence suggests that CyPA is elevated in PE. This research aims to investigate the effect of recombinant human CyPA on trophoblast migration and invasion both in vitro and in vivo. Materials and

Methods

We detected the expression and localization of CyPA in human placenta and explored the effects of CyPA on cell migration and invasion on HTR8/SVneo cell. Additionally, the expression levels of matrix metalloproteinase (MMP)-2/9 and molecules in the p38/ERK/JNK signaling pathway were detected. We established a mouse model by injecting pregnant mice with recombinant human CyPA and measured blood pressure, albumin/creatinine ratio, fetal and placenta weight of mice. Moreover, we examined the placental histology and MMP-2/9 and p38/ERK/JNK expression. Key findings: Our

Significance

We proposed that CyPA could inhibit trophoblast migration and invasion both in vitro and in vivo, which was involved in PE development.

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