Claudin-5 levels are reduced in human end-stage cardiomyopalhy
Claudin-5 levels are reduced in human end-stage cardiomyopalhy
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DOI：
10.1016/j.yjmcc.2008.04.005
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发表时间：
2008-07-01
影响因子：
5
通讯作者：
Rafael-Fortney, Jill A.
中科院分区：
文献类型：
--
作者：
Mays, Tessily A.;Binkley, Philip F.;Rafael-Fortney, Jill A.
Claudin-5 is a transmembrane cell junction protein that is a component of fight junctions in endothelial cell layers. We have previously shown that claudin-5 also localizes to lateral membranes of murine cardiomyocytes at their junction with the extracellular matrix. Claudin-5 levels are specifically reduced in myocytes from a mouse model of muscular dystrophy with cardiomyopathy. To establish whether claudin-5 is similarly specifically reduced in human cardiomyopathy, we compared the levels of claudin-5 with other cell junction proteins in 62 cardiomyopathic end-stage explant samples. We show that claudin-5 levels are reduced in at least 60% of patient samples compared with non-failing controls. Importantly, claudin-5 reductions can be independent of connexin-43, a gap junction protein previously reported to be reduced in failing heart samples. Other cell junction proteins including alpha-catenin, beta-catenin, gamma-catenin, desmoplakin, and N-cadherin are reduced in only a small number of failing samples and only in combination with reduced claudin-5 or connexin-43 levels. We also show that reduced claudin-5 levels can be present independently from dystrophin alterations, which are known to be capable of causing and resulting from cardiomyopathy. These data are the first to show alterations of a tight junction protein in human cardiomyopathy samples and suggest that claudin-5 may participate in novel mechanisms in the pathway to end-stage heart failure. (C) 2008 Elsevier Inc. All rights reserved.
