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  5. Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ
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Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/18711
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dc.contributor.authorOrrington-Myers, J.en
dc.contributor.authorGao, X.en
dc.contributor.authorKouklis, P.en
dc.contributor.authorBroman, M.en
dc.contributor.authorRahman, A.en
dc.contributor.authorVogel, S. M.en
dc.contributor.authorMalik, A. B.en
dc.date.accessioned2015-11-24T18:54:38Z-
dc.date.available2015-11-24T18:54:38Z-
dc.identifier.issn1040-0605-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/18711-
dc.rightsDefault Licence-
dc.subjectAdherens Junctions/physiologyen
dc.subjectAnimalsen
dc.subjectAntigens, CD/genetics/metabolism/*physiologyen
dc.subjectCadherins/genetics/metabolism/*physiologyen
dc.subjectCapillary Permeability/physiologyen
dc.subjectEndothelium, Vascular/*metabolismen
dc.subjectIntercellular Adhesion Molecule-1/metabolismen
dc.subjectLipopolysaccharides/pharmacologyen
dc.subjectLung/blood supply/drug effects/*physiologyen
dc.subjectMaleen
dc.subjectMiceen
dc.subjectMice, Inbred Strainsen
dc.subjectMicrocirculationen
dc.subjectMutationen
dc.subjectNF-kappa B/metabolismen
dc.subjectNeutrophil Infiltration/*physiologyen
dc.subjectProtein Structure, Tertiaryen
dc.subjectTransfectionen
dc.titleRegulation of lung neutrophil recruitment by VE-cadherinen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primary10.1152/ajplung.00502.2005-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/16782751-
heal.identifier.secondaryhttp://ajplung.physiology.org/content/291/4/L764.full.pdf-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2006-
heal.abstractLung inflammatory disease is characterized by increased polymorphonuclear leukocyte (PMN) infiltration and vascular permeability. PMN infiltration into tissue involves signaling between endothelial cells and migrating PMNs, which leads to alterations in the organization of adherens junctions (AJs). We addressed the possible role of the protein constituents of AJs, endothelium-specific vascular-endothelial (VE)-cadherin, in the migration of PMNs. Studies were made using VE-cadherin mutant constructs lacking the extracellular domain (DeltaEXD) or, additionally, lacking the COOH-terminus beta-catenin-binding domain (DeltaEXDDeltabeta). Either construct was transduced in pulmonary microvessel endothelia of mice using cationic liposome-encapuslated cDNA constructs injected intravenously. Optimal expression of constructs was seen by Western blot analysis within 24 h. Vessel wall liquid permeability measured as the lung microvessel capillary filtration coefficient increased threefold in DeltaEXD-transduced lungs, indicating patency of interendothelial junctions, whereas the control DeltaEXDDeltabeta construct was ineffective. To study lung tissue PMN recruitment, we challenged mice intraperitoneally with LPS (3 mg/kg) for 6 h and measured PMN numbers by bronchoalveolar lavage and their accumulation morphometrically in lung tissue. DeltaEXD expression markedly reduced the PMN sequestration and migration seen in nontransfected (control wild type) or DeltaEXDDeltabeta-transfected (negative control) mice challenged with LPS. In addition, DeltaEXD transfection suppressed LPS-induced activation of NF-kappaB and consequent ICAM-1 expression. These results suggest that disassembly of VE-cadherin junctions serves as a negative signal for limiting transendothelial PMN migration secondary to decreased ICAM-1 expression in the mouse model of LPS-induced sepsis.en
heal.journalNameAm J Physiol Lung Cell Mol Physiolen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
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