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J Thorac Cardiovasc Surg 2005;130:1326-1332
© 2005 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology

The remote ischemic preconditioning stimulus modifies gene expression in mouse myocardium

Igor E. Konstantinov, MD, PhD a , * , Sara Arab, PhD c , * , Jia Li, MD, PhD b , John G. Coles, MD a , Cathy Boscarino, MSc a , Alessandro Mori, BSc a , Eva Cukerman, BSc c , Fayez Dawood, DVM c , Michael M.H. Cheung, MD b , Mikiko Shimizu, MD c , Peter P. Liu, MD c , Andrew N. Redington, MD b , *

a Division of Cardiovascular Surgery, The Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada
b Division of Cardiology, The Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada
c Richard Lewar Centre of Excellence, Toronto General Hospital, University of Toronto, Toronto, Ontario, Canada

Received for publication January 10, 2005; revisions received February 24, 2005; accepted for publication March 23, 2005.

* Address for reprints: Andrew N. Redington, MD, Division of Cardiology, The Hospital for Sick Children, 555 University Ave, Toronto, M5G 1X8, Canada (Email: andrew.redington{at}sickkids.ca).

BACKGROUND: We have recently demonstrated that remote ischemic preconditioning reduces ischemia-reperfusion injury in animal models. The mechanisms by which the remote ischemic preconditioning stimulus exerts its effect remain to be fully defined, and its effect on myocardial gene expression is unknown. We tested the hypothesis that remote ischemic preconditioning modifies myocardial gene expression immediately after the remote ischemic preconditioning stimulus (early phase) and 24 hours later (late phase).

METHODS: Twenty male (C57BL/6) 10- to 12-week-old mice were randomized into 4 groups: group 1 (control, early phase; n = 5), group 2 (remote ischemic preconditioning, early phase; n = 5), group 3 (control, late phase; n = 5), and group 4 (remote ischemic preconditioning, late phase; n = 5). Groups 2 and 4 underwent remote ischemic preconditioning induced by 6 cycles of 4 minutes of occlusion and 4 minutes of reperfusion of the femoral artery. Groups 1 and 2 were killed 15 minutes after completion of sham procedure or remote ischemic preconditioning, and the hearts were removed and frozen in liquid nitrogen. Groups 3 and 4 were killed 24 hours after remote ischemic preconditioning, and the hearts were harvested in the same fashion. Gene expression was assessed by using the Affymetrix MG-430A chip (Affymetrix, Santa Clara, Calif).

RESULTS: Data filtering (P < .05, analysis of variance) and hierarchic 2-way clustering identified significant differences in gene expression among the 4 groups. Genes involved in protection against oxidative stress (eg, Hadhsc, Prdx4, and Fabp4) and cytoprotection (Hsp73) were upregulated, whereas many proinflammatory genes (eg, Egr-1 and Dusp 1 and 6) were suppressed.

CONCLUSION: A simple remote ischemic preconditioning stimulus modifies myocardial gene expression by upregulating cardioprotective genes and suppressing genes potentially involved in the pathogenesis of ischemia-reperfusion injury.

Abbreviations and Acronyms CNBP = cellular nucleic acid–binding protein; CPB = cardiopulmonary bypass; DUSP = dual-specificity phosphatase; FABP = fatty acid–binding protein; GAPDH = glyceraldehyde-3-phosphate dehydrogenase; HADHSC = L-3-hydroxyacyl-CoA dehydrogenase; HSP = heat shock protein; IPC = ischemic preconditioning; IR = ischemia-reperfusion; KIF = kinesin superfamily protein; PCR = polymerase chain reaction; PDGFRB = platelet-derived growth factor receptor ß; PPAR = peroxisome proliferator–activated receptor; rIPC = remote ischemic preconditioning; ROS = reactive oxygen species; SER = sarcoendoplasmic reticulum




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