ArticleThe Journal of clinical investigation2013
Reversal of gene dysregulation in cultured cytotrophoblasts reveals possible causes of preeclampsia.
Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 72 papers, 3 of them syntheses that pooled it.
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Who cites it
72 citing papers in PubMed, 3 syntheses or guidelines pooled it, 141 citations in OpenAlex.
- Current approaches and developments in transcript profiling of the human placenta.Human reproduction update · 2020Pooled it
- Glycogen synthase kinase (GSK) 3 in pregnancy and parturition: a systematic review of literature.The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians · 2020Pooled it
- Gestational tissue transcriptomics in term and preterm human pregnancies: a systematic review and meta-analysis.BMC medical genomics · 2015Pooled it
- Spatial Logic and Evolutionary Innovation in Human Placentation.bioRxiv : the preprint server for biology · 2026Article
- Integrative bioinformatics analysis identifies placental senescence-associated signatures in early-onset preeclampsia.Frontiers in endocrinology · 2026Article
- METTL3 safeguards cell identity and epigenome of human trophoblast stem cells.Nature communications · 2025Article
- Autophagy in PE: Dispute, Role and Potential Target.Cell proliferation · 2025Review
- Profiling the cytotoxic effects of naled and other pesticides in primary human placental cytotrophoblasts.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Epigenetic Changes Regulating Epithelial-Mesenchymal Plasticity in Human Trophoblast Differentiation.Cells · 2025Article
- Inhibition of placental trophoblast fusion by guanylate-binding protein 5.Science advances · 2025Article
- Two decades of advances in preeclampsia research: molecular mechanisms and translational studies.The Journal of clinical investigation · 2024Article
- Aging-regulated PNUTS maintains endothelial barrier function via SEMA3B suppression.Communications biology · 2024Article
- Article
- Potential Roles of microRNAs for Assessing Cardiovascular Risk in Pre-Eclampsia-Exposed Postpartum Women and Offspring.International journal of molecular sciences · 2023Review
- Immunoexpression of neuropilin-1 in the chorionic villi of HIV-infected preeclamptic South African women of African ancestry.Histochemistry and cell biology · 2023Article
- Cell-free DNA methylome analysis for early preeclampsia prediction.Nature medicine · 2023Article
- Elevated galectin-3 levels detected in women with hyperglycemia during early and mid-pregnancy antagonizes high glucose - induced trophoblast cells apoptosis via galectin-3/foxc1 pathway.Molecular medicine (Cambridge, Mass.) · 2023Article
- Paradoxical expression of NRP1 in decidual stromal and immune cells reveals a novel inflammation balancing mechanism during early pregnancy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Laminin switches terminal differentiation fate of human trophoblast stem cells under chemically defined culture conditions.The Journal of biological chemistry · 2023Article
- Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
During human pregnancy, a subset of placental cytotrophoblasts (CTBs) differentiates into cells that aggressively invade the uterus and its vasculature, anchoring the progeny and rerouting maternal blood to the placenta. In preeclampsia (PE), CTB invasion is limited, reducing placental perfusion and/or creating intermittent flow. This syndrome, affecting 4%-8% of pregnancies, entails maternal vascular alterations (e.g., high blood pressure, proteinuria, and edema) and, in some patients, fetal growth restriction. The only cure is removal of the faulty placenta, i.e., delivery. Previously, we showed that defective CTB differentiation contributes to the placental component of PE, but the causes were unknown. Here, we cultured CTBs isolated from PE and control placentas for 48 hours, enabling differentiation and invasion. In various severe forms of PE, transcriptomics revealed common aberrations in CTB gene expression immediately after isolation, including upregulation of SEMA3B, which resolved in culture. The addition of SEMA3B to normal CTBs inhibited invasion and recreated aspects of the PE phenotype. Additionally, SEMA3B downregulated VEGF signaling through the PI3K/AKT and GSK3 pathways, effects that were observed in PE CTBs. We propose that, in severe PE, the in vivo environment dysregulates CTB gene expression; the autocrine actions of the upregulated molecules (including SEMA3B) impair CTB differentiation, invasion and signaling; and patient-specific factors determine the signs.
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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.