ArticleThe Journal of clinical investigation2019
Lymphatic mimicry in maternal endothelial cells promotes placental spiral artery remodeling.
Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
32 citing papers in PubMed, 57 citations in OpenAlex.
- Select Histochemical and Immunohistochemical Methods to Investigate the Cell and Tissue Composition of the Mouse Placenta and Metrial Gland.Toxicologic pathology · 2026Review
- Article
- Single-Cell-Resolution Fate Mapping Reveals Embryonic Venous Origins of Fenestrated Hindbrain Choroid Plexus Vasculature.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- 3D imaging of the pregnant uterus reveals an extensively invasive mouse placenta and early CXCL12-CXCR4 requirement.bioRxiv : the preprint server for biology · 2026Article
- Placental Steroid Hormones in Preeclampsia: Multilayered Regulation of Endocrine Pathogenesis.Endocrine reviews · 2026Review
- Dipeptidylpeptidase 4 inhibition attenuates gestational pathologies via immune homeostasis restoration in the pulmonary-uterine axis.Nature communications · 2026Article
- Preeclampsia is Associated with Altered Expression of Ferroptosis Biomarkers in Placental but not Maternal Vasculature.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- sFlt-1/PlGF and beyond: angiolymphatic-associated signatures and emerging biomarkers in placental pathology.Vascular biology (Bristol, England) · 2025Review
- Preventing periprosthetic osteolysis in aging populations through lymphatic activation and stem cell-associated secretory phenotype inhibition.Communications biology · 2024Article
- Penile cavernous sinusoids are Prox1-positive hybrid vessels.Vascular biology (Bristol, England) · 2024Article
- Endocytosis at the maternal-fetal interface: balancing nutrient transport and pathogen defense.Frontiers in immunology · 2024Review
- The Effects of Preeclamptic Milieu on Cord Blood Derived Endothelial Colony-Forming Cells.bioRxiv : the preprint server for biology · 2023Article
- Endometrial TGFβ signaling fosters early pregnancy development by remodeling the fetomaternal interface.American journal of reproductive immunology (New York, N.Y. : 1989) · 2023Review
- Stromal cells-specific retinoic acid determines parturition timing at single-cell and spatial-temporal resolution.iScience · 2023Article
- Three-Dimensional Histological Characterization of the Placental Vasculature Using Light Sheet Microscopy.Biomolecules · 2023Article
- Article
- Vascular changes in the cycling and early pregnant uterus.JCI insight · 2023Review
- Roles of immune microenvironment in the female reproductive maintenance and regulation: novel insights into the crosstalk of immune cells.Frontiers in immunology · 2023Review
- Article
- Inhibition of Heme Oxygenase-1 by Zinc Protoporphyrin IX Improves Adverse Pregnancy Outcomes in Malaria During Early Gestation.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
Molecular heterogeneity of endothelial cells underlies their highly specialized functions during changing physiological conditions within diverse vascular beds. For example, placental spiral arteries (SAs) undergo remarkable remodeling to meet the ever-growing demands of the fetus - a process which is deficient in preeclampsia. The extent to which maternal endothelial cells coordinate with immune cells and pregnancy hormones to promote SA remodeling remains largely unknown. Here we found that remodeled SAs expressed the lymphatic markers PROX1, LYVE1, and VEGFR3, mimicking lymphatic identity. Uterine natural killer (uNK) cells, which are required for SA remodeling and secrete VEGFC, were both sufficient and necessary for VEGFR3 activation in vitro and in mice lacking uNK cells, respectively. Using Flt4Chy/+ mice with kinase inactive VEGFR3 and Vegfcfl/fl Vav1-Cre mice, we demonstrated that SA remodeling required VEGFR3 signaling, and that disrupted maternal VEGFR3 signaling contributed to late-gestation fetal growth restriction. Collectively, we identified a novel instance of lymphatic mimicry by which maternal endothelial cells promote SA remodeling, furthering our understanding of the vascular heterogeneity employed for the mitigation of pregnancy complications such as fetal growth restriction and preeclampsia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.