ArticleThe American journal of pathology2015
Placental fractalkine is up-regulated in severe early-onset preeclampsia.
Article in The American journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 48 citations in OpenAlex.
- Single-Cell Analysis of Preeclamptic Cord Blood Mononuclear Cells Revealed Activation of Heme-Associated Signalling Pathways.Journal of cellular and molecular medicine · 2026Article
- Fractalkine (Chemokine CX3CL1) Signaling During Placentation and Placental Function.International journal of molecular sciences · 2026Review
- Preeclampsia prediction and diagnosis: a comprehensive historical review from clinical insights to omics perspectives.Frontiers in medicine · 2025Review
- Establishment of a placental lncRNA-mRNA expression network for early-onset preeclampsia.BMC pregnancy and childbirth · 2024Article
- CX3CL1 (Fractalkine)-CX3CR1 Axis in Inflammation-Induced Angiogenesis and Tumorigenesis.International journal of molecular sciences · 2024Review
- The regulated cell death at the maternal-fetal interface: beneficial or detrimental?Cell death discovery · 2024Review
- The pathogenesis of obstetric APS: a 2023 update.Clinical immunology (Orlando, Fla.) · 2023Review
- Pathophysiological impact of CXC and CX3CL1 chemokines in preeclampsia and gestational diabetes mellitus.Frontiers in cell and developmental biology · 2023Review
- Placental dysfunction influences fetal monocyte subpopulation gene expression in preterm birth.JCI insight · 2022Article
- Role of chemokines in early pregnancy loss.Experimental and therapeutic medicine · 2022Article
- The potential association between a new angiogenic marker fractalkine and a placental vascularization in preeclampsia.Archives of gynecology and obstetrics · 2021Observational
- Insight into the Key Points of Preeclampsia Pathophysiology: Uterine Artery Remodeling and the Role of MicroRNAs.International journal of molecular sciences · 2021Review
- Is there an inflammatory stimulus to human term labour?PloS one · 2021Article
- Data-driven discovery of mid-pregnancy immune markers associated with maternal lifetime stress: results from an urban pre-birth cohort.Stress (Amsterdam, Netherlands) · 2020Article
- Platelet-derived factors impair placental chorionic gonadotropin beta-subunit synthesis.Journal of molecular medicine (Berlin, Germany) · 2020Article
- Overexpression of fractalkine and its histopathological characteristics in primary pterygium.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2019Article
- Maternal Platelets—Friend or Foe of the Human Placenta?International journal of molecular sciences · 2019Review
- Regulation of CX3CL1 Expression in Human First-Trimester Decidual Cells: Implications for Preeclampsia.Reproductive sciences (Thousand Oaks, Calif.) · 2019Article
- Placental CX3CL1 is Deregulated by Angiotensin II and Contributes to a Pro-Inflammatory Trophoblast-Monocyte Interaction.International journal of molecular sciences · 2019Article
- Downregulation of p53 drives autophagy during human trophoblast differentiation.Cellular and molecular life sciences : CMLS · 2018Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
The pathogenesis of preeclampsia (PE) includes the release of placental factors into the maternal circulation, inducing an inflammatory environment in the mother. One of the factors may be the proinflammatory chemokine fractalkine, which is expressed in the syncytiotrophoblast of human placenta, from where it is released into the maternal circulation by constitutive shedding. We examined whether placental fractalkine is up-regulated in severe early-onset PE and whether the proinflammatory cytokines tumor necrosis factor (TNF)-α and IL-6 are able to increase the expression of fractalkine. Gene expression analysis, enzyme-linked immunosorbent assay, and immunohistochemistry consistently showed increased fractalkine expression in placentas from severe early-onset PE, compared to gestational age-matched controls. Expression of a disintegrin and metalloproteinases (ADAMs) 10 and 17, which convert transmembrane fractalkine into the soluble form, was significantly increased in these cases. Incubation of first-trimester placental explants with TNF-α provoked a significant increase in fractalkine expression and release of the soluble form, whereas IL-6 had no effect. TNF-α-mediated up-regulation of placental fractalkine was reversed in the presence of the aspirin-derivative salicylate, which impaired activation of NF-κB p65 in TNF-α-treated explants. On the basis of data from placental explants, we suggest that increased maternal TNF-α may up-regulate the expression and release of placental fractalkine, which, in turn, may contribute to an exaggerated systemic inflammatory response in PE.
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