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Am J Physiol Heart Circ Physiol 279: H3020-H3030, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 6, H3020-H3030, December 2000

Interaction between angiotensin II and Smad proteins in fibroblasts in failing heart and in vitro

Jianming Hao, Baiqiu Wang, Stephen C. Jones, Davinder S. Jassal, and Ian M. C. Dixon

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

Angiotensin II (angiotensin) and transforming growth factor (TGF)-beta 1 play an important role in cardiac fibrosis. We examined Smad proteins in 8-wk post-myocardial infarction (MI) rat hearts. AT1 blockade (losartan) attenuated the activation of TGF-beta 1 in target tissues. Losartan administration (8 wk, 15 mg · kg-1 · day-1) normalized total Smad 2 overexpression in infarct scar and remnant heart tissue and normalized Smad 4 in infarct scar. Phosphorylated Smad 2 (P-Smad 2) staining decreased in cytosol from failing heart vs. the control, which was normalized by losartan, suggesting augmented P-Smad 2 movement into nuclei in untreated failing hearts. Using adult primary rat fibroblasts treated with angiotensin (10-6 M), we noted rapid translocation (15 min) of P-Smad 2 into the nuclei from the cytosol. Nuclear P-Smad 2 protein level increased with angiotensin treatment, which was blocked by losartan. We conclude that angiotensin may influence total Smad 2 and 4 expression in post-MI heart failure and that angiotensin treatment is associated with rapid P-Smad 2 nuclear translocation in isolated fibroblasts. This study suggests that cross talk between angiotensin and Smad signaling is associated with fibrotic events in post-MI hearts.

heart failure; myocardial infarction; cytokine


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