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Articles in PresS, published online ahead of print January 17, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00266.2001
Submitted on April 3, 2001
Accepted on January 8, 2002
1 Physiology, Institute of Cardiovascular Sciences, University of Manitoba, Winnipeg, MB, Canada
* To whom correspondence should be addressed. E-mail: iand{at}sbrc.umanitoba.ca.
We examined the role of TGF-ß1 signaling inhibitor Smad 7 in cardiac fibrosis. TGF-ß1 (10
g/ml) was found to increase cytosolic Smad 7 expression in primary adult rat fibroblasts and induce rapid nuclear export of exogenous Smad 7 in COS-7 cells. Furthermore, overexpression of Smad 7 in primary adult fibroblasts was associated with suppressed collagen type I and type III expression. We detected Smad 7, phosphorylated Smad 2, TGF-ß type I receptor (TßRI) and TGF-ß1 proteins in post-myocardial infarct (MI) rat hearts. In 2 wk and 4 wk post-MI hearts, Smad 7 and TßRI expression were decreased in scar tissue while TGF-ß1 expression was increased in scar and viable tissue. In the 8 wk post-MI heart, Smad 7 expression was decreased in both scar tissue and myocardium remote to the infarct scar. Finally, we confirmed that these changes are paralleled by decreased expression of cytosolic phosphorylated R-Smad 2 in 4 wk viable myocardium, and in 2 wk and 4 wk infarct scar tissues. Taken together, our data imply that decreased I-Smad 7 signal in cardiac fibroblasts may play a role in the pathogenesis of cardiac fibrosis in post-MI heart.
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