1999
DOI: 10.1111/j.1540-8167.1999.tb00645.x
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Abstract: Cx43 undergoes both distribution and concentration changes following acute cardiac ischemia. The loss of Cx43 protein is heterogeneous. Cx43 dephosphorylation occurred within 1 hour following ischemia.

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Cited by 68 publications
(46 citation statements)
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“…On the basis of these findings, we believe that proteolysis rather than "epitope masking by dephosphorylaiton" causes the "reduced immunostaining for Cx43 in ischemic myocardium". 2,3) Additionally, these changes precede the development of myocardial injury as demonstrated by the negative myoglobin diffusion or reduced triphenyltetrazolium chloride staining (data not shown), in the same model in which these changes can be reproduced after ischemia-reperfusion or prolonged ischemia (data not shown).…”
Section: Discussionmentioning
confidence: 74%
See 1 more Smart Citation
“…On the basis of these findings, we believe that proteolysis rather than "epitope masking by dephosphorylaiton" causes the "reduced immunostaining for Cx43 in ischemic myocardium". 2,3) Additionally, these changes precede the development of myocardial injury as demonstrated by the negative myoglobin diffusion or reduced triphenyltetrazolium chloride staining (data not shown), in the same model in which these changes can be reproduced after ischemia-reperfusion or prolonged ischemia (data not shown).…”
Section: Discussionmentioning
confidence: 74%
“…Cx43 immunoreactivity lies primarily in the intercalated discs (ID) and its intensity is reduced during myocardial ischemia, 2,3) which may implicate it arrhythmogenesis. 4) In Cx43-deficient mice, ischemia promotes ventricular arrhythmias.…”
mentioning
confidence: 99%
“…Nevertheless, other studies suggest that a fairly prolonged period of ischaemia is required (i.e. more than 1h) to observe significant Cx43 degradation [125]. In this respect, our results are in accordance with those studies, which demonstrated that Cx43 dephosphorylation may occur, without a net loss of protein level after a 40 min period of ischaemia [43].…”
Section: The Role Of Gap Junctions In the Delayed Phase Of Preconditisupporting
confidence: 93%
“…Transient activation of the sympathetic nervous system usually causes lethal arrhythmias in a diseased heart. Interestingly, disrupted gap-junction structure and decreased expression of Cx43 are also frequently seen in cardiac remodeling in response to various pathologic stimuli, such as ischemia, chronic pressure and volume overload in dogs [7] , guinea pigs [8] and humans [9] . However, little information concerning the relationship between sympathetic www.chinaphar.com Xia Y et al Acta Pharmacologica Sinica npg nervous system activation and functional regulation of myocardial gap junctions is available.…”
Section: Introductionmentioning
confidence: 99%