Limited forward trafficking of connexin 43 reduces cell-cell coupling in stressed human and mouse myocardium.

ABSTRACT: Gap junctions form electrical conduits between adjacent myocardial cells, permitting rapid spatial passage of the excitation current essential to each heartbeat. Arrhythmogenic decreases in gap junction coupling are a characteristic of stressed, failing, and aging myocardium, but the mechanisms of decreased coupling are poorly understood. We previously found that microtubules bearing gap junction hemichannels (connexons) can deliver their cargo directly to adherens junctions. The specificity of this delivery requires the microtubule plus-end tracking protein EB1. We performed this study to investigate the hypothesis that the oxidative stress that accompanies acute and chronic ischemic disease perturbs connexon forward trafficking. We found that EB1 was displaced in ischemic human hearts, s

SUBMITTER: Smyth JW 

PROVIDER: S-EPMC2798685 | biostudies-literature | 2010 Jan

REPOSITORIES: biostudies-literature