Placenta · 2025
Fibroblast growth factor 7 facilitates invasion of human trophoblast cells through the JNK pathway during pregnancy.
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Li Lijuan, Zhou Yu, Zhou Wenjie, Liu Yang, Mei Jie
Аннотация
INTRODUCTION: This study investigates the role of FGF7 in trophoblast invasion under high estrogen and progesterone levels, focusing on the JNK signaling pathway. The aim is to demonstrate that FGF7 enhances human trophoblast cell invasion via JNK activation, crucial for establishing pregnancy.
METHODS: We investigated the expression of FGF7 in primary human trophoblasts to evaluate the effects of elevated estrogen and progesterone levels on trophoblast invasion. The study focused on the role of FGF7 in gestational regulation and its mechanism of activating the JNK signaling pathway through FGFR2.
RESULTS: The study unveiled that FGF7 and FGFR2 are expressed in trophoblast cells during normal pregnancies, with the expression of FGF7 being upregulated by estrogen and progesterone. In trophoblastic cells, FGF7 activates the MAPK/JNK signaling pathway, resulting in upregulation of MMP-2 and MMP-9 expression, concomitant downregulation of TIMP-1 and TIMP-2 expression, and ultimately enhanced invasive capacity. However, in cases of recurrent spontaneous abortion (RSA), the levels of FGF7/FGFR2 expression exhibited a notable decrease. These results indicate that the involvement of FGF7/FGFR2 could be significant in maintaining normal pregnancy by regulating trophoblast invasiveness, and their impaired expression could contribute to RSA.
DISCUSSION: The present study elucidates the role of FGF7 in facilitating trophoblast invasion through activation of the MAPK/JNK pathway and upregulation of MMPs, thereby providing potential therapeutic insights for recurrent spontaneous abortion (RSA) attributed to impaired trophoblast invasion.
METHODS: We investigated the expression of FGF7 in primary human trophoblasts to evaluate the effects of elevated estrogen and progesterone levels on trophoblast invasion. The study focused on the role of FGF7 in gestational regulation and its mechanism of activating the JNK signaling pathway through FGFR2.
RESULTS: The study unveiled that FGF7 and FGFR2 are expressed in trophoblast cells during normal pregnancies, with the expression of FGF7 being upregulated by estrogen and progesterone. In trophoblastic cells, FGF7 activates the MAPK/JNK signaling pathway, resulting in upregulation of MMP-2 and MMP-9 expression, concomitant downregulation of TIMP-1 and TIMP-2 expression, and ultimately enhanced invasive capacity. However, in cases of recurrent spontaneous abortion (RSA), the levels of FGF7/FGFR2 expression exhibited a notable decrease. These results indicate that the involvement of FGF7/FGFR2 could be significant in maintaining normal pregnancy by regulating trophoblast invasiveness, and their impaired expression could contribute to RSA.
DISCUSSION: The present study elucidates the role of FGF7 in facilitating trophoblast invasion through activation of the MAPK/JNK pathway and upregulation of MMPs, thereby providing potential therapeutic insights for recurrent spontaneous abortion (RSA) attributed to impaired trophoblast invasion.