ArticleeLife2022
VE-cadherin enables trophoblast endovascular invasion and spiral artery remodeling during placental development.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Associations Between Follicular Fluid Biomarkers and IVF/ICSI Outcomes in Normo-Ovulatory Women-A Systematic Review.Biomolecules · 2025Pooled it
- A perfusable first-generation endometrial microvascular model to study human spiral artery remodeling in pregnancy.Lab on a chip · 2026Article
- Spatio-temporal expression of E-cadherin mediates trophoblast lineage transitions during human placentation.Molecular biology reports · 2026Review
- Understanding physiological adaptations of pregnancy to the chronic hypoxia of high altitude to inform obstetrical and neonatal care.Physiological reviews · 2026Review
- Taxifolin Inhibits Invasion and Endovascular Differentiation of Extravillous Trophoblast HTR-8/SVneo Cells.Cells · 2026Article
- Checkpoint kinase 2 coordinates autophagy activation and Aurora kinase A degradation to regulate primary cilia for cell invasion.Cell communication and signaling : CCS · 2026Article
- Cross-species insights into placental evolution and diseases at the single-cell resolution.Nature communications · 2026Article
- Dll4 assembles the umbilical cord and placental vasculature.JCI insight · 2026Article
- Tissue-Derived Extracellular Vesicles Define Diagnostic Biomarkers for Renal Cell Carcinoma.Journal of extracellular vesicles · 2026Article
- miR-142-3p regulates RDH13 to impair trophoblast function via regulating CDH5/LFA-1/L-SELECTIN axis: a novel mechanism and diagnostic/therapeutic for pre-eclampsia.Frontiers in medicine · 2026Article
- Distinct immune responses to HIV and CMV in Hofbauer cells across gestation highlight evolving placental immune dynamics.Frontiers in immunology · 2026Article
- Maternal high-fat, high-sucrose diet-induced excess adiposity is linked to placental hypoxia and disruption of fetoplacental immune homeostasis in late gestation†.Biology of reproduction · 2025Article
- mScience China. Life sciences · 2025Article
- Exploring the Relevance of S100A8 and S100A9 Proteins in Preeclampsia: A Narrative Review.International journal of molecular sciences · 2025Review
- Lineage tracing studies suggest that the placenta is not a de novo source of hematopoietic stem cells.PLoS biology · 2025Article
- Crosstalk between decidual natural killer cells and extravillous trophoblasts at the maternal-fetal interface: current status and future perspectives.Frontiers in immunology · 2025Review
- DOCK1 deficiency drives placental trophoblast cell dysfunction by influencing inflammation and oxidative stress, hallmarks of preeclampsia.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Article
- Rational Design of Nanomedicine for Placental Disorders: Birthing a New Era in Women's Reproductive Health.Small (Weinheim an der Bergstrasse, Germany) · 2024Review
- Preeclampsia in the Context of COVID-19: Mechanisms, Pathophysiology, and Clinical Outcomes.American journal of reproductive immunology (New York, N.Y. : 1989) · 2024Review
- High-throughput methylome analysis reveals differential methylation for early and late onset preeclampsia for mothers and their children.Physiological genomics · 2024Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
During formation of the mammalian placenta, trophoblasts invade the maternal decidua and remodel spiral arteries to bring maternal blood into the placenta. This process, known as endovascular invasion, is thought to involve the adoption of functional characteristics of vascular endothelial cells (ECs) by trophoblasts. The genetic and molecular basis of endovascular invasion remains poorly defined, however, and whether trophoblasts utilize specialized endothelial proteins in an analogous manner to create vascular channels remains untested. Vascular endothelial (VE-)cadherin is a homotypic adhesion protein that is expressed selectively by ECs in which it enables formation of tight vessels and regulation of EC junctions. VE-cadherin is also expressed in invasive trophoblasts and is a prime candidate for a molecular mechanism of endovascular invasion by those cells. Here, we show that VE-cadherin is required for trophoblast migration and endovascular invasion into the maternal decidua in the mouse. VE-cadherin deficiency results in loss of spiral artery remodeling that leads to decreased flow of maternal blood into the placenta, fetal growth restriction, and death. These studies identify a non-endothelial role for VE-cadherin in trophoblasts during placental development and suggest that endothelial proteins may play functionally unique roles in trophoblasts that do not simply mimic those in ECs.
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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.