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dc.contributor.authorTansey, Erin E.
dc.contributor.authorKwaku, Kevin F.
dc.contributor.authorHammer, Peter
dc.contributor.authorCowan, Douglas Burr
dc.contributor.authorFederman, Micheline
dc.contributor.authorLevitsky, Sidney
dc.contributor.authorMcCully, James Donald
dc.date.accessioned2016-06-20T20:29:09Z
dc.date.issued2006
dc.identifier.citationTansey, Erin E., Kevin F. Kwaku, Peter E. Hammer, Douglas B. Cowan, Micheline Federman, Sidney Levitsky, and James D. McCully. 2006. “Reduction and Redistribution of Gap and Adherens Junction Proteins After Ischemia and Reperfusion.” The Annals of Thoracic Surgery 82 (4) (October): 1472–1479. doi:10.1016/j.athoracsur.2006.04.061.en_US
dc.identifier.issn0003-4975en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:27357261
dc.description.abstractBackground Previous studies have demonstrated that alterations in myocardial structure, consistent with tissue and sarcomere disruption as well as myofibril dissociation, occur after myocardial ischemia and reperfusion. In this study we determine the onset of these structural changes and their contribution to electrical conduction. Methods Langendorff perfused rabbit hearts (n = 47) were subjected to 0, 5, 10, 15, 20, 25, and 30 minutes global ischemia, followed by 120 minutes reperfusion. Hemodynamics were recorded and tissue samples were collected for histochemical and immunohistochemical studies. Orthogonal epicardial conduction velocities were measured, with temperature controlled, in a separate group of 10 hearts subjected to 0 or 30 minutes of global ischemia, followed by 120 minutes of reperfusion. Results Histochemical and quantitative light microscopy spatial analysis showed significantly increased longitudinal and transverse interfibrillar separation after 15 minutes or more of ischemia (p < 0.05 versus control). Confocal immunohistochemistry and Western blot analysis demonstrated significant reductions (p < .05 versus control) of the intercellular adherens junction protein, N-cadherin, and the active phosphorylated isoform of the principal gap junction protein, connexin 43 at more than 15 minutes of ischemia. Cellular redistribution of connexin 43 was also evidenced on immunohistochemistry. No change in integrin-β1, an extracellular matrix attachment protein, or in epicardial conduction velocity anisotropy was observed. Conclusions These data indicate that there are significant alterations in the structural integrity of the myocardium as well as gap and adherens junction protein expression with increasing global ischemia time. The changes occur coincident with previously observed significant decreases in postischemic functional recovery, but are not associated with altered expression of matrix binding proteins or electrical anisotropic conduction.en_US
dc.language.isoen_USen_US
dc.publisherElsevier BVen_US
dc.relation.isversionofdoi:10.1016/j.athoracsur.2006.04.061en_US
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC1805692/en_US
dash.licenseLAA
dc.titleReduction and Redistribution of Gap and Adherens Junction Proteins After Ischemia and Reperfusionen_US
dc.typeJournal Articleen_US
dc.description.versionAccepted Manuscripten_US
dc.relation.journalThe Annals of Thoracic Surgeryen_US
dash.depositing.authorMcCully, James Donald
dc.date.available2016-06-20T20:29:09Z
dc.identifier.doi10.1016/j.athoracsur.2006.04.061*
dash.contributor.affiliatedFederman, Micheline
dash.contributor.affiliatedMcCully, James
dash.contributor.affiliatedHammer, Peter
dash.contributor.affiliatedCowan, Douglas
dash.contributor.affiliatedLevitsky, Sidney


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