ArticleThe Journal of biological chemistry2010
Cell-cell contact formation governs Ca2+ signaling by TRPC4 in the vascular endothelium: evidence for a regulatory TRPC4-beta-catenin interaction.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 49 citations in OpenAlex.
- The Molecular Heterogeneity of Store-Operated CaInternational journal of molecular sciences · 2023Review
- Polarized Proteins in Endothelium and Their Contribution to Function.Journal of vascular research · 2021Review
- STAT signaling in polycystic kidney disease.Cellular signalling · 2020Review
- Angiotensin-II-Evoked CaCells · 2020Article
- Lipid-independent control of endothelial and neuronal TRPC3 channels by light.Chemical science · 2019Article
- Targeting ELTD1, an angiogenesis marker for glioblastoma (GBM), also affects VEGFR2: molecular-targeted MRI assessment.American journal of nuclear medicine and molecular imaging · 2019Article
- Endothelial Transient Receptor Potential Channels and Vascular Remodeling: Extracellular CaFrontiers in physiology · 2019Review
- Functional Expression of TRP Ion Channels in Endometrial Stromal Cells of Endometriosis Patients.International journal of molecular sciences · 2018Article
- GαScientific reports · 2018Article
- Significant contribution of TRPC6 channel-mediated CaJournal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2016Review
- Transient receptor potential channels in the vasculature.Physiological reviews · 2015Review
- TRP Channels Localize to Subdomains of the Apical Plasma Membrane in Human Fetal Retinal Pigment Epithelium.Investigative ophthalmology & visual science · 2015Article
- The construction of common and specific significance subnetworks of Alzheimer's disease from multiple brain regions.BioMed research international · 2015Article
- The Roles of Rasd1 small G proteins and leptin in the activation of TRPC4 transient receptor potential channels.Channels (Austin, Tex.) · 2015Review
- Single-cell imaging of mechanotransduction in endothelial cells.Progress in molecular biology and translational science · 2014Review
- Effect of huanglian jiedu decoction on thoracic aorta gene expression in spontaneous hypertensive rats.Evidence-based complementary and alternative medicine : eCAM · 2014Article
- Enhanced CaJournal of nanomaterials · 2013Article
- Novel pyrazole compounds for pharmacological discrimination between receptor-operated and store-operated Ca(2+) entry pathways.British journal of pharmacology · 2012Article
- Update on vascular endothelial Ca(2+) signalling: A tale of ion channels, pumps and transporters.World journal of biological chemistry · 2012Article
- The Ca(2+) sensor stromal interaction molecule 1 (STIM1) is necessary and sufficient for the store-operated Ca(2+) entry function of transient receptor potential canonical (TRPC) 1 and 4 channels in endothelial cells.Molecular pharmacology · 2012Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TRPC4 is well recognized as a prominent cation channel in the vascular endothelium, but its contribution to agonist-induced endothelial Ca(2+) entry is still a matter of controversy. Here we report that the cellular targeting and Ca(2+) signaling function of TRPC4 is determined by the state of cell-cell adhesions during endothelial phenotype transitions. TRPC4 surface expression in human microvascular endothelial cells (HMEC-1) increased with the formation of cell-cell contacts. Epidermal growth factor recruited TRPC4 into the plasma membrane of proliferating cells but initiated retrieval of TRPC4 from the plasma membrane in quiescent, barrier-forming cells. Epidermal growth factor-induced Ca(2+) entry was strongly promoted by the formation of cell-cell contacts, and both siRNA and dominant negative knockdown experiments revealed that TRPC4 mediates stimulated Ca(2+) entry exclusively in proliferating clusters that form immature cell-cell contacts. TRPC4 co-precipitated with the junctional proteins beta-catenin and VE-cadherin. Analysis of cellular localization of fluorescent fusion proteins provided further evidence for recruitment of TRPC4 into junctional complexes. Analysis of TRPC4 function in the HEK293 expression system identified beta-catenin as a signaling molecule that enables cell-cell contact-dependent promotion of TRPC4 function. Our results place TRPC4 as a Ca(2+) entry channel that is regulated by cell-cell contact formation and interaction with beta-catenin. TRPC4 is suggested to serve stimulated Ca(2+) entry in a specific endothelial state during the transition from a proliferating to a quiescent phenotype. Thus, TRPC4 may adopt divergent, as yet unappreciated functions in endothelial Ca(2+) homeostasis and emerges as a potential key player in endothelial phenotype switching and tuning of cellular growth factor signaling.
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