Zonula occludens‐1 and connexin 43 expression in the failing human heart

S Kostin - Journal of cellular and molecular medicine, 2007 - Wiley Online Library
S Kostin
Journal of cellular and molecular medicine, 2007Wiley Online Library
Focal disorganization of gap junctional distribution and down‐regulation of the major gap
junctional protein connexin 43 are typical features of myocardial remodelling in the failing
human heart. Increasing evidence indicates that connexin 43 interacts with zonula‐
occludens‐1 (ZO‐1), and it has recently been shown that ZO‐1 promotes the formation and
growth of gap junctional plaques. In the present study, distribution patterns of ZO‐1 and
connexin 43 were studied in normal and in heart failure patients using double‐label …
Abstract
Focal disorganization of gap junctional distribution and down‐regulation of the major gap junctional protein connexin 43 are typical features of myocardial remodelling in the failing human heart. Increasing evidence indicates that connexin 43 interacts with zonula‐occludens‐1 (ZO‐1), and it has recently been shown that ZO‐1 promotes the formation and growth of gap junctional plaques. In the present study, distribution patterns of ZO‐1 and connexin 43 were studied in normal and in heart failure patients using double‐label immunohistochemistry and confocal microscopy. ZO‐1 was found to be co‐localized with connexin 43 at intercalated disks. Importantly, in patients with heart failure due to dilated or ischaemic cardimyopathy, areas of diminished connexin 43 expression were characterized by a markedly reduced ZO‐1 staining. Based on these data it is concluded that in patients with heart failure, down‐regulation of ZO‐1 matches the diminished expression levels of connexin 43, suggesting that ZO‐1 plays an important role in gap junction formation and gap junction plaque stability.
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