ArticleEndocrine, metabolic & immune disorders drug targets2024
PF4 Silencing Promotes Trophoblast Cell Proliferation, Migration, Invasion and EMT by Regulating SOCS3/STAT3 Signaling Pathway.
Article in Endocrine, metabolic & immune disorders drug targets, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- mBiochemical genetics · 2026Article
- Association between three lipid-lowering drugs and amnesia: a real-world pharmacovigilance study.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Platelets induce epithelial to mesenchymal transition in renal proximal tubular epithelial cells through TGF-β signaling pathway.Molecular medicine (Cambridge, Mass.) · 2025Article
- Identification and validation of ANXA3 and SOCS3 as biomarkers for acute myocardial infarction related to sphingolipid metabolism.Hereditas · 2025Article
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4 authors.
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Abstract
backgroundRecurrent Miscarriage (RM) is a chronic and heterogeneous autoimmune disease. Platelet factor 4 (PF4) has been found to be involved in the pathogenesis of RM.
objectiveWe aimed to explore the role and mechanism of PF4 on trophoblasts in RM in vitro.
methodsIn this study, the expression of PF4 and PF4 receptor CXC chemokine receptor 3 (CXCR3) in the placentas of patients with RM were analyzed by RT-qPCR and western blotting. Serum PF4 level was tested by ELISA. Following PF4 silencing and SOCS3 overexpression in HTR-8/SVneo cells, cell proliferation was detected by CCK-8, colony formation, and EDU assays. Wound healing and transwell assays separately evaluated cell migration and invasion. Immunofluorescence assay determined E-cadherin expression. Tube formation assay was used to measure the angiogenesis. Western blotting examined the expression of metastasis, epithelial-mesenchymal transition (EMT) and suppressor of cytokine signaling 3 (SOCS3)/signal transducer and activator of transcription 3 (STAT3) signaling-associated proteins.
resultsThe results revealed that PF4 displayed increased expression in placental villus tissues of RM patients. Serum PF4 level was also elevated in RM patients. PF4 silencing promoted the proliferation, migration, invasion, EMT, and angiogenesis of HTR-8/SVneo cells. Additionally, PF4 knockdown downregulated SOCS3 expression to activate STAT3 signaling. SOCS3 overexpression countervailed the effects of PF4 deficiency on HTR-8/SVneo cells.
conclusionIn summary, PF4 participated in the proliferation, migration, invasion, EMT and angiogenesis of trophoblast cells by modulating the SOCS3/STAT3 signaling pathway, indicating that targeting the PF4/SOCS3/STAT3 pathway could be a novel therapy for RM.
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