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Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/18586
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dc.contributor.authorGao, X.en
dc.contributor.authorKouklis, P.en
dc.contributor.authorXu, N.en
dc.contributor.authorMinshall, R. D.en
dc.contributor.authorSandoval, R.en
dc.contributor.authorVogel, S. M.en
dc.contributor.authorMalik, A. B.en
dc.date.accessioned2015-11-24T18:53:39Z-
dc.date.available2015-11-24T18:53:39Z-
dc.identifier.issn1040-0605-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/18586-
dc.rightsDefault Licence-
dc.subjectAdherens Junctions/drug effects/metabolismen
dc.subjectAnimalsen
dc.subjectAntibodies, Monoclonal/pharmacologyen
dc.subjectAntigens, CDen
dc.subjectCadherins/analysis/immunology/*metabolismen
dc.subjectCalcium/metabolismen
dc.subjectCapillary Permeability/physiologyen
dc.subjectCells, Cultureden
dc.subjectChelating Agents/pharmacologyen
dc.subjectEdetic Acid/pharmacologyen
dc.subjectElectric Impedanceen
dc.subjectEndothelium, Vascular/chemistry/cytology/*metabolismen
dc.subjectEpitopes/immunologyen
dc.subjectIodine Radioisotopes/diagnostic useen
dc.subjectLung/*blood supply/cytology/metabolismen
dc.subjectMaleen
dc.subjectMiceen
dc.subjectMice, Inbred Strainsen
dc.subjectOrgan Sizeen
dc.subjectPerfusionen
dc.subjectSerum Albumin, Bovine/pharmacokineticsen
dc.titleReversibility of increased microvessel permeability in response to VE-cadherin disassemblyen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/11076812-
heal.identifier.secondaryhttp://ajplung.physiology.org/content/279/6/L1218.full.pdf-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2000-
heal.abstractWe determined the role of vascular endothelial (VE)-cadherin complex in regulating the permeability of pulmonary microvessels. Studies were made in mouse lungs perfused with albumin-Krebs containing EDTA, a Ca(2+) chelator, added to study the VE-cadherin junctional disassembly. We then repleted the perfusate with Ca(2+) to restore VE-cadherin integrity. Confocal microscopy showed a disappearance of VE-cadherin immunostaining in a time- and dose-dependent manner after Ca(2+) chelation and reassembly of the VE-cadherin complex within 5 min after Ca(2+) repletion. We determined the (125)I-labeled albumin permeability-surface area product and capillary filtration coefficient (K(fc)) to quantify alterations in the pulmonary microvessel barrier. The addition of EDTA increased (125)I-albumin permeability-surface area product and K(fc) in a concentration-dependent manner within 5 min. The permeability response was reversed within 5 min after repletion of Ca(2+). An anti-VE-cadherin monoclonal antibody against epitopes responsible for homotypic adhesion augmented the increase in K(fc) induced by Ca(2+) chelation and prevented reversal of the response. We conclude that the disassembled VE-cadherins in endothelial cells are mobilized at the junctional plasmalemmal membrane such that VE-cadherins can rapidly form adhesive contact and restore microvessel permeability by reannealing the adherens junctions.en
heal.journalNameAm J Physiol Lung Cell Mol Physiolen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
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