title: Decreased expression of VE-cadherin and claudin-5 and increased phosphorylation of VE-cadherin in vascular endothelium in nasal polyps.
abstract: VE-cadherin and claudin-5 are major components of adherens and tight junctions of vascular endothelial cells and a decrease in their expression and an increase in the tyrosine-phosphorylation of VE-cadherin are associated with an increase in endothelial paracellular permeability. To clarify the mechanism underlying the development of edema in nasal polyps, we studied these molecules in polyp microvessels. Normal inferior turbinate mucosal tissues and nasal polyps from patients treated with or without glucocorticoid were stained for VE-cadherin or claudin-5 and CD31 by a double-immunofluorescence method and the immunofluorescence intensities were graded 1-3 with increasing intensity. To correct for differences in fluorescence intensity attributable to a different endothelial area being exposed in a section or to the thickness of a section, the relative immunofluorescence intensity was estimated by dividing the grade of VE-cadherin or claudin-5 by that of CD31 in each microvessel. Tyrosine-phosphorylation of VE-cadherin was examined by Western blot analysis. The relative intensities of VE-cadherin and claudin-5 in the CD31-positive microvessels significantly decreased in the following order; inferior turbinate mucosa, treated polyps and untreated polyps. The ratio of tyrosine-phosphorylated VE-cadherin to VE-cadherin was significantly higher in untreated polyps than in the inferior turbinate mucosa and treated polyps, between which no significant difference in the ratio was seen. Thus, in nasal polyps, the barrier function of endothelial adherens and tight junctions is weakened, although glucocorticoid treatment improves this weakened barrier function.
authors.affiliation: Department of Pathology, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo, 663-8501, Japan.
authors.forename: Yoriko
authors.initials: Y
authors.lastname: Yukitatsu
authors.forename: Masaki
authors.initials: M
authors.lastname: Hata
authors.forename: Koji
authors.initials: K
authors.lastname: Yamanegi
authors.forename: Naoko
authors.initials: N
authors.lastname: Yamada
authors.forename: Hideki
authors.initials: H
authors.lastname: Ohyama
authors.forename: Keiji
authors.initials: K
authors.lastname: Nakasho
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Kojima
authors.forename: Hideki
authors.initials: H
authors.lastname: Oka
authors.forename: Kenzo
authors.initials: K
authors.lastname: Tsuzuki
authors.forename: Masafumi
authors.initials: M
authors.lastname: Sakagami
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Terada
mesh_terms: D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000378:metabolism*; D015820:Cadherins / Q000378:metabolism*; D062507:Claudin-5 / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000378:metabolism*; D005260:Female; D005453:Fluorescence; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009298:Nasal Polyps / Q000378:metabolism* / Q000473:pathology; D009504:Neutrophils / Q000378:metabolism; D010766:Phosphorylation; D019000:Phosphotyrosine / Q000378:metabolism; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D033921:Vesicular Transport Proteins / Q000378:metabolism; D000099152:Cadherin 5
chemical_list: D015703:Antigens, CD; D015820:Cadherins; D062507:Claudin-5; D019000:Phosphotyrosine; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D033921:Vesicular Transport Proteins; D000099152:Cadherin 5; C119248:LYVE1 protein, human