ArticleJCI insight2019
Faulty oxygen sensing disrupts angiomotin function in trophoblast cell migration and predisposes to preeclampsia.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 39 citations in OpenAlex.
- STOX1 Promotes Pyroptosis of Hypoxic Trophoblast Cells Via the Nrf2/Caspase-1 Axis.Molecular reproduction and development · 2026Article
- Research trajectory of the mechanism of preeclampsia: a scientometric perspective.Journal of health, population, and nutrition · 2025Article
- Exploring the Role of Lower Genital Tract Microbiota and Cervical-Endometrial Immune Metabolome in Unknown Genesis of Recurrent Pregnancy Loss.International journal of molecular sciences · 2025Observational
- NADLife science alliance · 2024Article
- Streamlined Analysis of Maternal Plasma Indicates Small Extracellular Vesicles are Significantly Elevated in Early-Onset Preeclampsia.Reproductive sciences (Thousand Oaks, Calif.) · 2024Article
- Research Progress on Extracellular Matrix Involved in the Development of Preeclampsia.Current protein & peptide science · 2024Review
- Circulating and Endometrial Profiles of miR-145, miR-155-5p, miR-224, MPP-5, and PECAM-1 Expression in Patients with Repeated Implantation Failure: A Case Control Study.Cell journal · 2023Article
- The X-factor in ART: does the use of assisted reproductive technologies influence DNA methylation on the X chromosome?Human genomics · 2023Article
- Distinct Changes in Placental Ceramide Metabolism Characterize Type 1 and 2 Diabetic Pregnancies with Fetal Macrosomia or Preeclampsia.Biomedicines · 2023Article
- HIF1 inhibitor acriflavine rescues early-onset preeclampsia phenotype in mice lacking placental prolyl hydroxylase domain protein 2.JCI insight · 2022Article
- Widespread hydroxylation of unstructured lysine-rich protein domains by JMJD6.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Human Chorionic Villous Differentiation and Placental Development.International journal of molecular sciences · 2022Review
- Autism Spectrum Disorder from the Womb to Adulthood: Suggestions for a Paradigm Shift.Journal of personalized medicine · 2021Review
- JMJD6 Dysfunction Due to Iron Deficiency in Preeclampsia Disrupts Fibronectin Homeostasis Resulting in Diminished Trophoblast Migration.Frontiers in cell and developmental biology · 2021Article
- Role of A Novel Angiogenesis FKBPL-CD44 Pathway in Preeclampsia Risk Stratification and Mesenchymal Stem Cell Treatment.The Journal of clinical endocrinology and metabolism · 2021Article
- Increased placental mitochondrial fusion in gestational diabetes mellitus: an adaptive mechanism to optimize feto-placental metabolic homeostasis?BMJ open diabetes research & care · 2020Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Human placenta development and a successful pregnancy is incumbent upon precise oxygen-dependent control of trophoblast migration/invasion. Persistent low oxygen leading to failed trophoblast invasion promotes inadequate spiral artery remodeling, a characteristic of preeclampsia. Angiomotin (AMOT) is a multifaceted scaffolding protein involved in cell polarity and migration, yet its upstream regulation and significance in the human placenta remain unknown. Herein, we show that AMOT is primarily expressed in migratory extravillous trophoblast cells (EVTs) of the intermediate and distal anchoring column. Its expression increases after 10 weeks of gestation when oxygen tension rises and EVT migration/invasion peaks. Time-lapse imaging confirmed that the AMOT 80-kDa isoform promotes migration of trophoblastic JEG3 and HTR-8/SVneo cells. In preeclampsia, however, AMOT expression is decreased and its localization to migratory fetomaternal interface EVTs is disrupted. We demonstrate that Jumonji C domain-containing protein 6 (JMJD6), an oxygen sensor, positively regulates AMOT via oxygen-dependent lysyl hydroxylation. Furthermore, in vitro and ex vivo studies show that transforming growth factor-β (TGF-β) regulates AMOT expression, its interaction with polarity protein PAR6, and its subcellular redistribution from tight junctions to cytoskeleton. Our data reveal an oxygen- and TGF-β-driven migratory function for AMOT in the human placenta, and implicate its deficiency in impaired trophoblast migration that plagues preeclampsia.
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