The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians · 2026
Prokineticin 2 is upregulated in preeclampsia and impairs trophoblast function.
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Li Ying, Qin Ting, Long Xi-Gui, Wei Hai-Tang, Chi Yan
Аннотация
OBJECTIVE: To investigate the role of prokineticin 2 (PK2) in the pathogenesis of preeclampsia (PE), a severe hypertensive disorder of pregnancy with incompletely understood placental mechanisms.
METHODS: The placental expression of PK2 and prokineticin receptor 2 (PKR2) was assessed by immunohistochemistry, and PK2 levels were quantified by enzyme-linked immunosorbent assay in samples from patients with PE and a PE mouse model, compared with normal controls. The functional impact of recombinant PK2 protein on proliferation and migration was assessed in the trophoblast cell line HTR-8/SVneo. Transcriptomic analysis was performed on PK2-treated cells to identify differentially expressed genes and enriched pathways.
RESULTS: PK2 and PKR2 were significantly upregulated in PE placentas. PK2 expression was significantly higher in the culture medium of primary trophoblast cells derived from PE patients and a PE mouse model than in that from normal controls. Recombinant PK2 markedly inhibited trophoblast proliferation and migration. Transcriptomic analysis revealed PK2-induced upregulation of a gene set (including EGR1, FOS, JUN, CCN1, and CCN2) with significant enrichment in stress-response and inflammatory pathways.
CONCLUSIONS: This study identifies PK2 as a key pathogenic factor in PE that impairs trophoblast function. The findings suggest that its mechanism may involve the induction of AP-1 components. Our work provides the first evidence positioning the PK2/PKR2 axis as a novel contributor to PE pathogenesis and a potential therapeutic target.
METHODS: The placental expression of PK2 and prokineticin receptor 2 (PKR2) was assessed by immunohistochemistry, and PK2 levels were quantified by enzyme-linked immunosorbent assay in samples from patients with PE and a PE mouse model, compared with normal controls. The functional impact of recombinant PK2 protein on proliferation and migration was assessed in the trophoblast cell line HTR-8/SVneo. Transcriptomic analysis was performed on PK2-treated cells to identify differentially expressed genes and enriched pathways.
RESULTS: PK2 and PKR2 were significantly upregulated in PE placentas. PK2 expression was significantly higher in the culture medium of primary trophoblast cells derived from PE patients and a PE mouse model than in that from normal controls. Recombinant PK2 markedly inhibited trophoblast proliferation and migration. Transcriptomic analysis revealed PK2-induced upregulation of a gene set (including EGR1, FOS, JUN, CCN1, and CCN2) with significant enrichment in stress-response and inflammatory pathways.
CONCLUSIONS: This study identifies PK2 as a key pathogenic factor in PE that impairs trophoblast function. The findings suggest that its mechanism may involve the induction of AP-1 components. Our work provides the first evidence positioning the PK2/PKR2 axis as a novel contributor to PE pathogenesis and a potential therapeutic target.