Key result
Heart failure of various etiologies in animal models was associated with significant increases in inhibitory G protein (Gi) levels (15-35% increases, p<0.05) compared to controls.
Why the study?
Does heart failure increase the levels and function of inhibitory G protein (Gi) in the myocardium of animal models?
Does heart failure increase the levels and function of inhibitory G protein (Gi) in the myocardium of animal models?
Inhibitory G protein (Gi) levels and function are increased in the myocardium across various animal models of heart failure, suggesting its role in altered signal transduction in this condition.
Gi protein changes vary by species and HF etiology in animal models; leaves open optimal preclinical model selection for translation.
To identify any differences in inhibitory G protein (Gi) attributable to species or the cause of heart failure, we studied the changes in this protein in different animal models of heart failure: 1) different species; rats vs. hamsters (F1B) with cardiomyopathy induced by adriamycin (ADR) and 2) different etiologies; rats with ischemic heart failure (IHD) due to coronary artery ligation vs. rats with cardiomyopathy induced by ADR and F1B (20-week-old) hamsters with cardiomyopathy induced by ADR vs Syrian hamsters BIO 14.6 (40-week-old) with genetic cardiomyopathy, using Western blotting methods and ADP-ribosylation. We also sought to determine whether changes in the amount of Gi protein reflected the regulation of adenylate cyclase. The amount of immunodetectable Gi rose by 35% (p < 0.05) in ADR rats, 25% (p < 0.05) in ADR hamsters, 15% (p < 0.05) in IHD rats, and 28% (p < 0.05) in BIO 14.6 hamsters, as compared with control rats, F1B (20-week-old) hamsters, sham-operated control rats, and F1B (40-week-old) hamsters, respectively. Assessment of Gi by pertussis toxin-catalyzed ADP-ribosylation revealed increases in Gi of 24% (p < 0.05) in ADR rats and of 44% (p < 0.05) in BIO 14.6 hamsters, as compared with their respective controls. Gi function, as assayed by the acetylcholine-induced inhibition of adenylate cyclase, also increased. Thus, Gi protein appears to contribute to the changes in signal transduction in myocardium with heart failure.
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Kawamoto et al. (1994) studied Heart failure. Heart failure (various etiologies) vs. Control rats, sham-operated control rats, and control hamsters was evaluated on Amount of immunodetectable Gi protein (p=< 0.05). Heart failure of various etiologies in animal models was associated with significant increases in inhibitory G protein (Gi) levels (15-35% increases, p<0.05) compared to controls.
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