ArticleAmerican journal of physiology. Heart and circulatory physiology2011
Temporal and spatial correlation of platelet-activating factor-induced increases in endothelial [Ca²⁺]i, nitric oxide, and gap formation in intact venules.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 18 citations in OpenAlex.
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- Interactions between Nitric Oxide and Hyaluronan Implicate the Migration of Breast Cancer Cells.Biomacromolecules · 2022Article
- Leveraging avidin-biotin interaction to quantify permeability property of microvessels-on-a-chip networks.American journal of physiology. Heart and circulatory physiology · 2022Article
- Oxidative Stress and Microvessel Barrier Dysfunction.Frontiers in physiology · 2020Review
- HPhysiological reports · 2019Article
- Gliclazide Prevents 5-FU-Induced Oral Mucositis by Reducing Oxidative Stress, Inflammation, and P-Selectin Adhesion Molecules.Frontiers in physiology · 2019Article
- Transendothelial movement of adiponectin is restricted by glucocorticoids.The Journal of endocrinology · 2017Article
- Reduction of Endothelial Nitric Oxide Increases the Adhesiveness of Constitutive Endothelial Membrane ICAM-1 through Src-Mediated Phosphorylation.Frontiers in physiology · 2017Article
- Calcium Signaling Is Dispensable for Receptor Regulation of Endothelial Barrier Function.The Journal of biological chemistry · 2016Article
- Inhibition of endothelial nitric oxide synthase decreases breast cancer cell MDA-MB-231 adhesion to intact microvessels under physiological flows.American journal of physiology. Heart and circulatory physiology · 2016Article
- Microperfusion Technique to Investigate Regulation of Microvessel Permeability in Rat Mesentery.Journal of visualized experiments : JoVE · 2015Article
- In vitro recapitulation of functional microvessels for the study of endothelial shear response, nitric oxide and [Ca2+]i.PloS one · 2015Article
- Enhanced permeability responses to inflammation in streptozotocin-induced diabetic rat venules: Rho-mediated alterations of actin cytoskeleton and VE-cadherin.American journal of physiology. Heart and circulatory physiology · 2014Article
- Caveolin-1 scaffolding domain promotes leukocyte adhesion by reduced basal endothelial nitric oxide-mediated ICAM-1 phosphorylation in rat mesenteric venules.American journal of physiology. Heart and circulatory physiology · 2013Article
- H2O2-induced endothelial NO production contributes to vascular cell apoptosis and increased permeability in rat venules.American journal of physiology. Heart and circulatory physiology · 2013Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
We have previously demonstrated that platelet-activating factor (PAF)-induced increases in microvessel permeability were associated with endothelial gap formation and that the magnitude of peak endothelial intracellular Ca(2+) concentration ([Ca(2+)](i)) and nitric oxide (NO) production at the single vessel level determines the degree of the permeability increase. This study aimed to examine whether the magnitudes of PAF-induced peak endothelial [Ca(2+)](i), NO production, and gap formation are correlated at the individual endothelial cell level in intact rat mesenteric venules. Endothelial gaps were quantified by the accumulation of fluorescent microspheres at endothelial clefts using confocal imaging. Endothelial [Ca(2+)](i) was measured on fura-2- or fluo-4-loaded vessels, and 4,5-diaminofluorescein (DAF-2) was used for NO measurements. The results showed that increases in endothelial [Ca(2+)](i), NO production, and gap formation occurred in all endothelial cells when vessels were exposed to PAF but manifested a spatial heterogeneity in magnitudes among cells in each vessel. PAF-induced peak endothelial [Ca(2+)](i) preceded the peak NO production by 0.6 min at the cellular level, and the magnitudes of NO production and gap formation linearly correlated with that of the peak endothelial [Ca(2+)](i) in each cell, suggesting that the initial levels of endothelial [Ca(2+)](i) determine downstream NO production and gap formation. These results provide direct evidence from intact venules that inflammatory mediator-induced increases in microvessel permeability are associated with the generalized formation of endothelial gaps around all endothelial cells. The spatial differences in the molecular signaling that were initiated by the heterogeneous endothelial Ca(2+) response contribute to the heterogeneity in permeability increases along the microvessel wall during inflammation.
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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.