ArticleJournal of assisted reproduction and genetics2022
Suppression of FPR2 expression inhibits inflammation in preeclampsia by improving the biological functions of trophoblast via NF-κB pathway.
Article in Journal of assisted reproduction and genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Defective Trophoblast Differentiation, Endothelial Dysfunction, and Immune Dysregulation in Preeclampsia Coalesce on a Placental VGLL3-Centered Gene Network.Circulation · 2026Article
- Endothelial microparticles in high glucose environment: molecular pathways of GDM-associated placental dysfunction and coenzyme Q10-based targeted therapy.Journal of nanobiotechnology · 2026Article
- RBM15 mediates m6A methylation modification of FOSB mRNA to promote dysfunction of trophoblast cells-a potential link to preeclampsia.Hereditas · 2025Article
- VGLL3-centered network connects placental, vascular, and immune defects in preeclampsia.bioRxiv : the preprint server for biology · 2025Article
- Formyl peptide receptor 2: a potential therapeutic target for inflammation-related diseases.Pharmacological reports : PR · 2025Review
- The NFκB Signaling Pathway Is Involved in the Pathophysiological Process of Preeclampsia.Geburtshilfe und Frauenheilkunde · 2024Article
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- Identification of ferroptosis, necroptosis, and pyroptosis-associated genes in periodontitis-affected human periodontal tissue using integrated bioinformatic analysis.Frontiers in pharmacology · 2022Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThe dysfunction of trophoblast during inflammation plays an important role in PE. Formyl peptide receptor 2 (FPR2) plays crucial roles in the development of inflammation-associated disease. This present study aimed to explore the effect of FPR2 on a trophoblast cellular model of preeclampsia.
methodsThe expression of FPR2 in placenta was detected by immunohistochemical staining and western blotting. Transfection of siRNA was used to knockdown FPR2 in HTR-8/SVneo cells. Inflammatory cytokines were detected by ELISA. CCK8, Transwell, wound healing, FACS and tube formation assays were performed to observe the abilities of cell proliferation, migration, invasion, apoptosis and angiogenesis. Western blotting was implemented to clarify that NF-κB signaling pathway was downstream of FPR2.
resultsThe expression levels of FPR2 were higher in placental tissues of patients with PE. Knockdown of FPR2 expression by siFPR2 or inhibition of its activity by WRW4 decreased the release of proinflammatory cytokines in HTR8/SVneo cells treated with LPS. Knockdown of FPR2 expression or inhibition of its activity further reversed the LPS-induced attenuation of the proliferation, migration, invasion and angiogenesis and increase in apoptosis in HTR8/SVneo cells. Moreover, the NF-κB signaling pathway was activated in both placental tissues of patients with PE and LPS-treated HTR8/SVneo cells. However, the activation was attenuated when FPR2 was knocked down or inhibited.
conclusionSuppression of FPR2 expression alleviated the effects of inflammation induced by LPS on trophoblasts via the NF-κB signaling pathway, which provided a novel and potential strategy for the treatment of PE.
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