Ischemia Enhances Translocation of Connexin43 and Gap Junction Intercellular Communication, Thereby Propagating Contraction Band Necrosis After Reperfusion

Connexin-43 Redistribution and Gap Junction Activation During Forced Restraint Protects Against Sudden Arrhythmic Death in Rats

“…27, 28 Heart homogenate was centrifuged at 1,000 × g for 10 min, and the supernatant was spun at 100,000 × g for 60 min. The 1,000 × g pellets, 100,000 × g pellets, and 100,000 × g supernatant are referred to as the P1, P2, and S fractions, respectively.…”

“…28 GJIC was examined in pairs of rats, one of which underwent IMO + CBX for 60 min, while the other served as a control (free movement). Transverse sections were excised from the apexes.…”

Gap Junctions Mediate the Spread of Ischemia-Reperfusion Injury

“…10 Consistent with these reports, the authors also found that inhibition of enhanced GJIC ameliorated membrane disruption during reperfusion and reduced the CBN area and infarct size in the reperfused heart, providing in vivo evidence that gap junctions mediate the spread of cell death after ischemia-reperfusion injury (Figure 2). 6 In contrast to these results, many animal studies have demonstrated that ischemic insults induce rapid dephosphorylation of Cx43 and thereby alter the distribution of gap junctions from intercalated disks to the sides of cardiomyocytes (referred to as lateralization). 2,11 These alterations are thought to contribute to electrical uncoupling that provokes ventricular arrhythmia during myocardial ischemia.…”

“…In this issue of the Circulation Journal, Shintani-Ishida et al 6 examine the role of GJIC in ischemia-reperfusion injury. They carefully estimated cellular localization of phosphorylated and dephosphorylated Cx43 in the ischemic heart by using the subcellular fractionation technique.…”

Does Remodeling of Gap Junctions and Connexin Expression Contribute to Arrhythmogenesis?

“…There was no translocation of hypoxia inducible factor-1α, and the distribution of Cx43 was different from that in ischemia. 8 Unuma et al concluded that translocation of Cx43 to the GJ-enriched fraction occurs via the α1-adrenoceptor pathway independently of ischemia. 7 The results provided by Unuma et al 7 are the first demonstration of α-adrenoreceptor-dependent Cx43 translocation to GJs in IMO rats.…”