HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Sidney Levitsky Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Tansey, E. E. Articles by McCully, J. D. Search for Related Content PubMed PubMed Citation Articles by Tansey, E. E. Articles by McCully, J. D. Related Collections Myocardial protection

Ann Thorac Surg 2006;82:1472-1479
© 2006 The Society of Thoracic Surgeons

---

Original Articles: Cardiovascular

Reduction and Redistribution of Gap and Adherens Junction Proteins After Ischemia and Reperfusion

^a Division of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center, Boston, Massachusetts
^b Division of Cardiology, Beth Israel Deaconess Medical Center, Boston, Massachusetts
^c Department of Pathology, Beth Israel Deaconess Medical Center, Boston, Massachusetts
^d Department of Anesthesiology, Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts

Accepted for publication April 19, 2006.

^_* Address correspondence to Dr McCully, Division of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, 77 Ave Louis Pasteur, Rm 144, Boston, MA 02115 (Email: james_mccully{at}hms.harvard.edu).

Presented at the Poster Session of the Forty-second Annual Meeting of The Society of Thoracic Surgeons, Chicago, IL, Jan 30-Feb 1, 2006.

BACKGROUND: 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-ß1, 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.

This article has been cited by other articles:

				I. K. Toumpoulis, J. T. Oxford, D. B. Cowan, C. E. Anagnostopoulos, C. K. Rokkas, T. P. Chamogeorgakis, D. C. Angouras, R. J. Shemin, M. Navab, M. Ericsson, et al. Differential expression of collagen type V and XI alpha-1 in human ascending thoracic aortic aneurysms. Ann. Thorac. Surg., August 1, 2009; 88(2): 506 - 513. [Abstract] [Full Text] [PDF]

				J. D. McCully, M. K. Bhasin, C. Daly, M. C. Guerrero, S. Dillon, T. A. Liberman, D. B. Cowan, J. D. Mably, F. X. McGowan, and S. Levitsky Transcriptomic and proteomic analysis of global ischemia and cardioprotection in the rabbit heart Physiol Genomics, July 9, 2009; 38(2): 125 - 137. [Abstract] [Full Text] [PDF]

				J. D. McCully, D. B. Cowan, C. A. Pacak, I. K. Toumpoulis, H. Dayalan, and S. Levitsky Injection of isolated mitochondria during early reperfusion for cardioprotection Am J Physiol Heart Circ Physiol, January 1, 2009; 296(1): H94 - H105. [Abstract] [Full Text] [PDF]

				M. Ream, A. M. Ray, R. Chandra, and D. M. Chikaraishi Early fetal hypoxia leads to growth restriction and myocardial thinning Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2008; 295(2): R583 - R595. [Abstract] [Full Text] [PDF]

				A. E. Zemljic-Harpf, J. C. Miller, S. A. Henderson, A. T. Wright, A. M. Manso, L. Elsherif, N. D. Dalton, A. K. Thor, G. A. Perkins, A. D. McCulloch, et al. Cardiac-Myocyte-Specific Excision of the Vinculin Gene Disrupts Cellular Junctions, Causing Sudden Death or Dilated Cardiomyopathy Mol. Cell. Biol., November 1, 2007; 27(21): 7522 - 7537. [Abstract] [Full Text] [PDF]