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Low Expression of Endothelial Claudin‐5 Correlates with Sites Vulnerable to Atherosclerosis
Author(s) -
Karamanian Armen A,
Davies Peter F
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a752-a
Subject(s) - claudin , occludin , tight junction , pathology , biology , endothelium , western blot , immunostaining , chemistry , anatomy , microbiology and biotechnology , immunohistochemistry , medicine , endocrinology , gene , genetics
Atherosclerosis‐susceptible arterial sites are associated with disturbed flow (DF) profiles and increased endothelial permeability. Claudin‐5 (CLDN5) is an endothelial specific tight junction molecule that influences the permeability of the endothelium. Endothelial cells were isolated from the inner curvature of the aortic arch (DF; athero‐susceptible) and a nearby undisturbed flow (UF) region of the descending thoracic aorta (UF; athero‐protected) of normal swine. Western blot analysis revealed a 5‐fold lower level of CLDN5 in DF compared to UF regions. Expression of Zonula Occludens‐1, Occludin and Claudin‐1 were similar at both locations. CLDN5 expression was weak by immunostaining in DF and prominent in UF regions. By en face confocal microscopy of intact artery, the distribution of CLDN5 was similar at both locations. Although flow has been shown to modulate endothelial permeability in vitro , little is known about its in vivo effects on tight junctions. Our data suggest that the low expression of CLDN5 in permeable DF regions may influence their spatial susceptibility to atherosclerosis. Supported by grants from the NHLBI