ArticleThe Journal of biological chemistry2014
Genome-wide approaches reveal functional vascular endothelial growth factor (VEGF)-inducible nuclear factor of activated T cells (NFAT) c1 binding to angiogenesis-related genes in the endothelium.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 68 citations in OpenAlex.
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- Calcineurin/NFATc1 pathway represses cellular cytotoxicity by modulating histone H3 expression.Scientific reports · 2024Article
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- Molecular basis and current insights of atypical Rho small GTPase in cancer.Molecular biology reports · 2024Review
- G protein subunit alpha i2's pivotal role in angiogenesis.Theranostics · 2024Article
- Cracking the Endothelial Calcium (CaInternational journal of molecular sciences · 2023Review
- Prevascularization techniques for dental pulp regeneration: potential cell sources, intercellular communication and construction strategies.Frontiers in bioengineering and biotechnology · 2023Review
- In Vitro Angiogenesis Inhibition and Endothelial Cell Growth and Morphology.International journal of molecular sciences · 2022Article
- Novel Role of Prereplication Complex Component Cell Division Cycle 6 in Retinal Neovascularization.Arteriosclerosis, thrombosis, and vascular biology · 2022Article
- Endothelial Notch signaling directly regulates the small GTPase RND1 to facilitate Notch suppression of endothelial migration.Scientific reports · 2022Article
- Nuclear factor of activated T-cells (NFAT) regulation of IL-1β-induced retinal vascular inflammation.Biochimica et biophysica acta. Molecular basis of disease · 2021Article
- The First WHO International Standard for Harmonizing the Biological Activity of Bevacizumab.Biomolecules · 2021Article
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
VEGF is a key regulator of endothelial cell migration, proliferation, and inflammation, which leads to activation of several signaling cascades, including the calcineurin-nuclear factor of activated T cells (NFAT) pathway. NFAT is not only important for immune responses but also for cardiovascular development and the pathogenesis of Down syndrome. By using Down syndrome model mice and clinical patient samples, we showed recently that the VEGF-calcineurin-NFAT signaling axis regulates tumor angiogenesis and tumor metastasis. However, the connection between genome-wide views of NFAT-mediated gene regulation and downstream gene function in the endothelium has not been studied extensively. Here we performed comprehensive mapping of genome-wide NFATc1 binding in VEGF-stimulated primary cultured endothelial cells and elucidated the functional consequences of VEGF-NFATc1-mediated phenotypic changes. A comparison of the NFATc1 ChIP sequence profile and epigenetic histone marks revealed that predominant NFATc1-occupied peaks overlapped with promoter-associated histone marks. Moreover, we identified two novel NFATc1 regulated genes, CXCR7 and RND1. CXCR7 knockdown abrogated SDF-1- and VEGF-mediated cell migration and tube formation. siRNA treatment of RND1 impaired vascular barrier function, caused RhoA hyperactivation, and further stimulated VEGF-mediated vascular outgrowth from aortic rings. Taken together, these findings suggest that dynamic NFATc1 binding to target genes is critical for VEGF-mediated endothelial cell activation. CXCR7 and RND1 are NFATc1 target genes with multiple functions, including regulation of cell migration, tube formation, and barrier formation in endothelial cells.
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