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Activin A, a member of the TGF\u2010<jats:italic>\u03b2<\/jats:italic> family, shares the same intra\u2010cellular Smad signalling pathway with TGF\u2010<jats:italic>\u03b2<\/jats:italic>, but binds to its own specific transmembrane receptors and to follistatin, a secreted protein that inhibits activin by sequestration. Recent studies provide evidences of a novel role of activin A in inflammatory and repair processes. The aim of this study was to evaluate the importance of activin A and follistatin expression in the different phases of scar evolution. Immunostaining of sections obtained from active phase hypertrophic scars (AHS) revealed the presence of a high number of <jats:italic>\u03b1<\/jats:italic>\u2010SMA<jats:sup>+<\/jats:sup> myofibroblasts and DC\u2010SIGN<jats:sup>+<\/jats:sup> dendritic cells coexpressing activin A. Ex\u2010vivo AHS fibroblasts produced more activin and less follistatin than normal skin or remission phase hypertrophic scar (HS) fibroblasts, both in basal conditions and upon TGF\u2010<jats:italic>\u03b2<\/jats:italic>s stimulation. We demonstrate that fibroblasts do express activin receptors, and that this expression is not affected by TGF\u2010<jats:italic>\u03b2<\/jats:italic>s. Treatment of HS fibroblasts with activin A induced Akt phosphorylation, promoted cell proliferation, and enhanced <jats:italic>\u03b1<\/jats:italic>\u2010SMA and type I collagen expression. Follistatin reduced proliferation and suppressed activin\u2010induced collagen expression. These results indicate that the activin\/follistatin interplay has a role in HS formation and evolution. The impact of these observations on the understanding of wound healing and on the identification of new therapeutic targets is discussed.<\/jats:p>","DOI":"10.1111\/j.1600-0625.2007.00571.x","type":"journal-article","created":{"date-parts":[[2007,6,16]],"date-time":"2007-06-16T13:58:27Z","timestamp":1182002307000},"page":"600-610","source":"Crossref","is-referenced-by-count":42,"title":["Imbalance between activin A and follistatin drives postburn hypertrophic scar formation in human 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