ArticlePloS one2012
Fibroblast growth factor signaling potentiates VE-cadherin stability at adherens junctions by regulating SHP2.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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.
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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.
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Who cites it
28 citing papers in PubMed, 56 citations in OpenAlex.
- Review
- LncRNA SNHG1 enhances cartilage regeneration by modulating chondrogenic differentiation and angiogenesis potentials of JBMMSCs via mitochondrial function regulation.Stem cell research & therapy · 2024Article
- FGF-2 promotes angiogenesis through a SRSF1/SRSF3/SRPK1-dependent axis that controls VEGFR1 splicing in endothelial cells.BMC biology · 2021Article
- The quiescent endothelium: signalling pathways regulating organ-specific endothelial normalcy.Nature reviews. Cardiology · 2021Review
- Permeability of the Endothelial Barrier: Identifying and Reconciling Controversies.Trends in molecular medicine · 2021Review
- Review
- Is all plasma created equal? A pilot study of the effect of interdonor variability.The journal of trauma and acute care surgery · 2020Article
- In vivo Screening of Natural Products Against Angiogenesis and Mechanisms of Anti-Angiogenic Activity of Deoxysappanone B 7,4'-Dimethyl Ether.Drug design, development and therapy · 2020Article
- FGF2, an Immunomodulatory Factor in Asthma and Chronic Obstructive Pulmonary Disease (COPD).Frontiers in cell and developmental biology · 2020Review
- Hypoxia induction in cultured pancreatic islets enhances endothelial cell morphology and survival while maintaining beta-cell function.PloS one · 2019Article
- SHP-2 is activated in response to force on E-cadherin and dephosphorylates vinculin Y822.Journal of cell science · 2018Article
- Identification of mundoserone by zebrafishExperimental and therapeutic medicine · 2018Article
- Developmental SMAD6 loss leads to blood vessel hemorrhage and disrupted endothelial cell junctions.Developmental biology · 2018Article
- Endothelial cell SHP-2 negatively regulates neutrophil adhesion and promotes transmigration by enhancing ICAM-1-VE-cadherin interaction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Aqueous humour concentrations of TGF-β, PLGF and FGF-1 and total retinal blood flow in patients with early non-proliferative diabetic retinopathy.Acta ophthalmologica · 2017Article
- The molecular basis of endothelial cell plasticity.Nature communications · 2017Review
- Modulation of VEGF receptor 2 signaling by protein phosphatases.Pharmacological research · 2017Review
- Interleukin 2 Activates Brain Microvascular Endothelial Cells Resulting in Destabilization of Adherens Junctions.The Journal of biological chemistry · 2016Article
- Fibroblast growth factor signaling in the vasculature.Current atherosclerosis reports · 2015Review
- CDH2 and CDH11 act as regulators of stem cell fate decisions.Stem cell research · 2015Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe fibroblast growth factor (FGF) system plays a critical role in the maintenance of vascular integrity via enhancing the stability of VE-cadherin at adherens junctions. However, the precise molecular mechanism is not well understood. In the present study, we aimed to investigate the detailed mechanism of FGF regulation of VE-cadherin function that leads to endothelial junction stabilization. METHODS AND
findingsIn vitro studies demonstrated that the loss of FGF signaling disrupts the VE-cadherin-catenin complex at adherens junctions by increasing tyrosine phosphorylation levels of VE-cadherin. Among protein tyrosine phosphatases (PTPs) known to be involved in the maintenance of the VE-cadherin complex, suppression of FGF signaling reduces SHP2 expression levels and SHP2/VE-cadherin interaction due to accelerated SHP2 protein degradation. Increased endothelial permeability caused by FGF signaling inhibition was rescued by SHP2 overexpression, indicating the critical role of SHP2 in the maintenance of endothelial junction integrity.
conclusionsThese results identify FGF-dependent maintenance of SHP2 as an important new mechanism controlling the extent of VE-cadherin tyrosine phosphorylation, thereby regulating its presence in adherens junctions and endothelial permeability.
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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.