© 1999 by European Society of Cardiology
Copyright © 1999, European Society of Cardiology
Expression of Gi-2
and Gs in myofibroblasts localized to the infarct scar in heart failure due to myocardial infarction
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
and Gs 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 and Gs 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 protein concentration occurs in the border and scar regions vs. control values, respectively, in 8-week post-MI rat hearts. Similarly, immunoreactive Gs 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 and Gs proteins were localized to myofibroblasts in the infarct scar and to viable myocytes bordering the scar. Northern analysis revealed that the Gi-2/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/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 and Gs 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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