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Cardiovascular Research 1999 41(3):575-585; doi:10.1016/S0008-6363(98)00264-8
© 1999 by European Society of Cardiology
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Copyright © 1999, European Society of Cardiology

Expression of Gi-2{alpha} and Gs{alpha} in myofibroblasts localized to the infarct scar in heart failure due to myocardial infarction

David J. Peterson, Haisong Ju, Jianming Hao, Marcello Panagia, Donald C. Chapman and Ian M.C. Dixon*

Molecular Cardiology Laboratory, Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Faculty of Medicine, University of Manitoba, 351 Tache Avenue, Winnipeg, Manitoba, Canada R2H 2A6

* Corresponding author. Tel. +1-204-235-3419; Fax: +1-204-233-6723; E-mail: iand@sbrc.umanitoba.ca

Objective: Patients surviving large transmural myocardial infarction (MI) are at risk for congestive heart failure with attendant alteration of ventricular geometry and scar remodeling. Altered Gi-2{alpha} and Gs{alpha} protein expression may be involved in cardiac remodeling associated with heart failure, however their expression in scar tissue remains unclear. Methods: MI was produced in Sprague–Dawley rats by ligation of the left coronary artery. Gi-2{alpha} and Gs{alpha} protein concentration, localization and mRNA abundance were noted in surviving left ventricle remote to the infarct, in border and in scar tissues from 8 week post-MI hearts with moderate heart failure. Results: We observed a 4.5- and 5.0-fold increase in immunoreactive Gi-2{alpha} protein concentration occurs in the border and scar regions vs. control values, respectively, in 8-week post-MI rat hearts. Similarly, immunoreactive Gs{alpha} protein concentration was increased 3.4- and 8.2-fold, respectively, in these tissues vs. controls. Double-fluorescence labeling and phenotyping studies revealed that both Gi-2{alpha} and Gs{alpha} proteins were localized to myofibroblasts in the infarct scar and to viable myocytes bordering the scar. Northern analysis revealed that the Gi-2{alpha}/GAPDH ratio was increased in both viable and scar regions (1.24- and 1.85-fold respectively) from experimental hearts when compared to sham-operated control values when compared to noninfarcted left ventricle, the value of this ratio in scar tissue was elevated ~1.5 fold. The Gs{alpha}/GAPDH ratio was significantly increased (1.28-fold) only in the scar region vs. control. Conclusion: Our results indicate a marked increase in the expression of Gi-2{alpha} and Gs{alpha} from myofibroblasts of the infarct scar as well as remnant myocytes bordering the scar in 8-week post-MI rat hearts. We suggest that these changes may be associated with ongoing remodeling in the infarct scar in chronic post-MI phase of this experimental model.

KEYWORDS Myofibroblasts; Gene expression; G-proteins; Congestive heart failure; Myocardial infarction; Scar; Remodeling; Immunofluorescence


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