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TGF-ß3 Decreases Type I Collagen and Scarring after Labioplasty

¹ Graduate School of Dental Science,
² Pediatric Dentistry, Division of Oral Health, Growth & Development, and
³ Division of Maxillofacial Diagnostic and Surgical Sciences, Faculty of Dental Science, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka 812-8582, Japan; and
⁴ Cartilage Biology and Orthopaedics Branch, National Institutes of Health, Bethesda, MD, USA;

*corresponding author, m-ohishi{at}dent.kyushu-u.ac.jp

Cleft lip is a common congenital malformation, and labioplasty performed on infants to repair such defects often results in severe scar formation. Since TGF-ß3 has been implicated in wound healing, we therefore hypothesized that TGF-ß3 functions to reduce scarring after cleft lip repair. In this investigation, we demonstrated that exogenous TGF-ß3 reduced scar formation in an incised and sutured mouse lip in vivo. During labioplasty, endogenous TGF-ß3 expression was also elevated. In vitro experiments showed that exogenous TGF-ß3 reduced type I collagen accumulation. Furthermore, TGF-ß3 inhibited alpha-smooth-muscle actin expression, a marker for myofibroblasts. In tandem, TGF-ß3 induced the expression and activity of MMP-9. Analysis of our data suggests that TGF-ß3 is normally secreted following labioplastic wound healing. An elevated level of TGF-ß3 reduces type I collagen deposition by restricting myofibroblast differentiation and thereby collagen synthesis, and by promoting collagen degradation by MMP-9. In combination, these events lead to TGF-ß3-mediated reduced scar formation.

KEY WORDS: cleft lip • CL/Fraser mouse • mesenchymal cells • myofibroblast • matrix metalloproteinase-9

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