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Low Expression of Claudin‐5, a flow‐sensitive endothelial tight junction molecule, correlates with sites vulnerable to atherosclerosis in vivo
Author(s) -
Karamanian Armen A,
Davies Peter F
Publication year - 2008
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.22.1_supplement.1120.12
Subject(s) - tight junction , occludin , claudin , cell junction , biology , paracellular transport , pathology , immunostaining , in vivo , permeability (electromagnetism) , chemistry , microbiology and biotechnology , immunology , immunohistochemistry , medicine , cell , biochemistry , genetics , membrane
In large arteries atherosclerosis‐susceptible sites are associated with disturbed flow (DF) while athero‐protected sites are associated with undisturbed (UF) flow. Increased endothelial permeability to macromolecules, a prominent feature in DF regions, is considered to contribute to this susceptibility. The main determinant of endothelial paracellular permeability is the tight junction, a group of proteins that seal the intercellular space. However, little is known about the tight junction responses to different flow profiles. Endothelial cells were isolated from two DF (aortic arch and renal branch) and UF (descending thoracic aorta and renal artery) regions from normal adult pigs and probed for expression of tight junction molecules. Western blots revealed a 5‐fold lower expression of Claudin‐5 (CLDN5) in DF compared to UF regions whereas expressions of Zonula Occludens‐1, Occludin and VE‐cadherin were not significantly different. In situ immunostaining of CLDN5 protein was weak in DF and prominent in UF regions. CLDN5 is a flow sensitive molecule and its low expression in DF regions of heightened permeability may influence spatial susceptibility to atherosclerosis. Supported by grants from the NHLBI.