ArticleMolecular and cellular endocrinology2020
Adenoviral transduction of EGFR into pregnancy-adapted uterine artery endothelial cells remaps growth factor induction of endothelial dysfunction.
Article in Molecular and cellular endocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Does the use of bisphosphonates during pregnancy affect fetal outcomes? A systematic review.European journal of clinical pharmacology · 2024Pooled it
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- Mechanism of the epidermal growth factor receptor in promoting endothelial cell dysfunction in gestational diabetes mellitus.World journal of diabetes · 2025Article
- Cholesterol deficiency directs autophagy-dependent secretion of extracellular vesicles.bioRxiv : the preprint server for biology · 2025Article
- Activation of coagulation FXI promotes endothelial inflammation and amplifies platelet activation in a nonhuman primate model of hyperlipidemia.Research and practice in thrombosis and haemostasis · 2024Article
- Circulating extracellular vesicles in healthy and pathological pregnancies: A scoping review of methodology, rigour and results.Journal of extracellular vesicles · 2023Article
- The epidermal growth factor receptor in healthy pregnancy and preeclampsia.Journal of molecular endocrinology · 2023Review
- IMP1/IGF2BP1 in human colorectal cancer extracellular vesicles.American journal of physiology. Gastrointestinal and liver physiology · 2022Article
- The Efficacy Mechanism of Epigallocatechin Gallate against Pre-Eclampsia based on Network Pharmacology and Molecular Docking.Reproductive sciences (Thousand Oaks, Calif.) · 2022Article
- The Role of Connexin in Ophthalmic Neovascularization and the Interaction between Connexin and Proangiogenic Factors.Journal of ophthalmology · 2022Review
- The Involvement of Cell Adhesion Molecules, Tight Junctions, and Gap Junctions in Human Placentation.Reproductive sciences (Thousand Oaks, Calif.) · 2021Review
- Extracellular vesicles in spontaneous preterm birth.American journal of reproductive immunology (New York, N.Y. : 1989) · 2021Review
- Integrated Analysis of Hub Genes and MicroRNAs in Human Placental Tissues fromFrontiers in endocrinology · 2021Article
- Potential mechanism of action ofRSC advances · 2020Article
- Extracellular Vesicles as Signaling Mediators and Disease Biomarkers across Biological Barriers.International journal of molecular sciences · 2020Review
- Extracellular Vesicles in Feto-Maternal Crosstalk and Pregnancy Disorders.International journal of molecular sciences · 2020Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
During pregnancy, uterine vascular vasodilation is enhanced through adapted Ca2+ signaling, facilitated through increased endothelial connexin 43 (Cx43) gap junctional communication (GJC). In preeclampsia (PE), this adaptive response is missing. Of note, the angiogenic factor VEGF can also act via Src and ERK to close Cx43 gap junctions. While VEGFR2 is necessary for such closure, a role VEGFR1 is less clear. We reasoned if VEGFR2 is acting alone, then substituting another growth factor receptor with VEGFR2-like signaling should have the same effect. In uterine artery endothelial cells derived from pregnant sheep (P-UAEC), endogenous EGFR expression is very low. When we used adenovirus to raise EGFR, we also dose-dependently induced EGF-sensitive Cx43 phosphorylation mainly via ERK, and corresponding loss of Ca2+ bursts, but eliminated VEGF effects on phosphorylation of Cx43 or loss of Ca2+ bursting. This surprising observation suggests that while activated EGFR may indeed substitute for VEGFR2, it also sequesters a limited pool of effector molecules needed for VEGFR2 to phosphorylate Cx43. Thus, low endogenous EGFR expression in P-UAEC may be a necessary strategy to allow VEGFR-2 control of GJC, a first step in initiating angiogenesis in healthy pregnancy. Of further note, trophoblasts are rich in EGFR, and we have demonstrated shed PLAP+/EGFR + extracellular vesicles in maternal circulation in first trimester plasma samples using nanoscale high resolution flow cytometry. Collectively our data suggest that placenta derived exosomes positive for EGFR should be further considered as a possible cause of endothelial dysfunction in women with PE.
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