ArticleArteriosclerosis, thrombosis, and vascular biology2015
Orai3 Surface Accumulation and Calcium Entry Evoked by Vascular Endothelial Growth Factor.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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
19 citing papers in PubMed, 29 citations in OpenAlex.
- A Rare Case of Polymicrogyria in an Elderly Individual With Unique Polygenic Underlining.Cureus · 2024Article
- Upregulation of Orai Channels Contributes to Aging-Related Vascular Alterations in Rat Coronary Arteries.International journal of molecular sciences · 2023Article
- New Insights into the Reparative Angiogenesis after Myocardial Infarction.International journal of molecular sciences · 2023Review
- p38 MAPK activation and STIM1-Orai3 association mediate TRPC6 externalization.American journal of physiology. Cell physiology · 2023Article
- The Molecular Heterogeneity of Store-Operated CaInternational journal of molecular sciences · 2023Review
- Novel Paracrine Action of Endothelium Enhances Glucose Uptake in Muscle and Fat.Circulation research · 2021Article
- Advances in Intracellular Calcium Signaling Reveal Untapped Targets for Cancer Therapy.Biomedicines · 2021Review
- Vascular Calcification Mechanisms: Updates and Renewed Insight into Signaling Pathways Involved in High Phosphate-Mediated Vascular Smooth Muscle Cell Calcification.Biomedicines · 2021Review
- The N terminus of Orai1 couples to the AKAP79 signaling complex to drive NFAT1 activation by local CaProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Role of Junctional Adhesion Molecule-C in the Regulation of Inner Endothelial Blood-Retinal Barrier Function.Frontiers in cell and developmental biology · 2021Article
- ORAI1 CaFrontiers in cell and developmental biology · 2021Review
- Divergent effects of genetic and pharmacological inhibition of Nox2 NADPH oxidase on insulin resistance-related vascular damage.American journal of physiology. Cell physiology · 2020Article
- Group 1 metabotropic glutamate receptors trigger glutamate-induced intracellular CaCellular and molecular life sciences : CMLS · 2020Article
- Endothelial CaInternational journal of molecular sciences · 2019Review
- Article
- Store-Operated CaCancers · 2019Review
- ORAI channels in cellular remodeling of cardiorespiratory disease.Cell calcium · 2019Review
- The TRPC5 channel regulates angiogenesis and promotes recovery from ischemic injury in mice.The Journal of biological chemistry · 2019Article
- The Role of Endothelial CaInternational journal of molecular sciences · 2018Review
Corrections and comments
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Authors and funding
21 authors at 1 institution in 1 country.
Funding
Abstract
objectiveVascular endothelial growth factor (VEGF) acts, in part, by triggering calcium ion (Ca(2+)) entry. Here, we sought understanding of a Synta66-resistant Ca(2+) entry pathway activated by VEGF. APPROACH AND
resultsMeasurement of intracellular Ca(2+) in human umbilical vein endothelial cells detected a Synta66-resistant component of VEGF-activated Ca(2+) entry that occurred within 2 minutes after VEGF exposure. Knockdown of the channel-forming protein Orai3 suppressed this Ca(2+) entry. Similar effects occurred in 3 further types of human endothelial cell. Orai3 knockdown was inhibitory for VEGF-dependent endothelial tube formation in Matrigel in vitro and in vivo in the mouse. Unexpectedly, immunofluorescence and biotinylation experiments showed that Orai3 was not at the surface membrane unless VEGF was applied, after which it accumulated in the membrane within 2 minutes. The signaling pathway coupling VEGF to the effect on Orai3 involved activation of phospholipase Cγ1, Ca(2+) release, cytosolic group IV phospholipase A2α, arachidonic acid production, and, in part, microsomal glutathione S-transferase 2, an enzyme which catalyses the formation of leukotriene C4 from arachidonic acid. Shear stress reduced microsomal glutathione S-transferase 2 expression while inducing expression of leukotriene C4 synthase, suggesting reciprocal regulation of leukotriene C4-synthesizing enzymes and greater role of microsomal glutathione S-transferase 2 in low shear stress.
conclusionsVEGF signaling via arachidonic acid and arachidonic acid metabolism causes Orai3 to accumulate at the cell surface to mediate Ca(2+) entry and downstream endothelial cell remodeling.
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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.