The gap junction uncoupler heptanol abrogates infarct size reduction with preconditioning in mouse hearts.
Authors:
Journal: Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology
Publication Type: Journal Article
Date: 2002
DOI: 10.1016/s1054-8807(02)00102-3
ID: 12031768
Abstract
Emerging evidence suggests that gap junction-mediated intercellular transmission of ions, metabolites and/or second messengers may serve as important determinants of myocyte viability. Our aim was to determine, using isolated buffer-perfused mouse hearts, whether the cardioprotection achieved with ischemic preconditioning (PC) is due in part to: (i) disruption of cell-cell coupling (manifest as a loss in the primary gap junction protein, connexin 43 [Cx43]) and resultant impaired transmission of a 'death' messenger, or conversely, (ii) transfer of a humoral 'survival' factor via existing gap junctions.
Chemical List
- Connexin 43|||Heptanol