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Institute for Molecular and Cellular Regulation (W.W., I.K.), Gunma University, Maebashi 371-8512; Department of General Surgical Science (W.W., H.K.), Gunma University Graduate School of Medicine; and School of Veterinary Medicine and Animal Science (Y.H.) Kitasato University, Towada 034-8628, Japan
Address all correspondence and requests for reprints to: Itaru Kojima, M.D., Institute for Molecular and Cellular Regulation, Gunma University, Maebashi 371-8512, Japan. E-mail: ikojima{at}showa.gunma-u.ac.jp.
The present study was conducted to examine the role of activin A in the activation of cultured rat hepatic stellate cells (HSC). HSC expressed mRNA for the ßA-subunit of activin and the type I and II activin receptors. TGF-ß increased the mRNA expression of the ßA-subunit of activin as well as the release of the ßA dimer, activin A. Exogenous activin A activated HSC and increased the expression of 
-smooth muscle actin and collagen. Exogenous follistatin, an antagonist of activin A, blocked not only the effect of activin A but also the effect of TGF-ß on the expression of type I collagen. Similarly, follistatin inhibited TGF-ß-induced secretion of collagen from HSC. Additionally, the effect of TGF-ß was markedly reduced in HSC overexpressing the dominant-negative type II activin receptor. In contrast, the effect of activin A on the collagen production was not affected in HSC overexpressing the dominant-negative type II TGF-ß receptor. In conclusion, an autocrine factor activin A mediates part of the action of TGF-ß on the production of collagen in HSC. The results also suggest that follistatin may be useful for the treatment of hepatic fibrosis.
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