title: Inhibitory effect of TGF-β peptide antagonist on the fibrotic phenotype of human hypertrophic scar fibroblasts.
abstract: BACKGROUND
  TGF-β plays a central role in hypertrophic scar (HS) formation and development.
  
  
  OBJECTIVE
  This study investigated the role of a TGF-β antagonist peptide in inhibiting fibrotic behavior of human HS-derived fibroblasts (HSFs).
  
  
  METHODS
  HSFs were seeded at a density of 3.1 × 10(4)/cm(2) and were subjected to treatment of peptide antagonist (30 μM) or TGF-β receptor inhibitor LY2109761 (10 μM) or without treatment followed by the analyses of quantitative PCR, Elisa, in vitro wounding and fibroblast-populated collagen lattice (FPCL) assays.
  
  
  RESULTS
  qPCR and Elisa analyses showed that the peptide could, respectively, reduce the gene (at 48 h) and protein (at 72 h) expression levels of collagen I (86 ± 4.8%; 56.6 ± 7.3%), collagen III (73 ± 10.7%; 43.7 ± 7.2%), fibronectin (90 ± 8.9%; 21.1 ± 2.8%), and TGF-β1 (85 ± 9.3%; 25.0 ± 9.4%) as opposed to the non-treated group (p < 0.05), as the LY2109761 group similarly did. Cell proliferation was also significantly inhibited at day 5 (CCK-8 assay) by both peptide and LY2109761 treatments compared with the non-treated group (p < 0.05). The peptide also significantly inhibited cell migration as opposed to blank control at 24 h (43 ± 6.7% versus 60 ± 2.1%, p < 0.05) and at 48 h (63.9 ± 3.1% versus 95 ± 4.1%, p < 0.05). Similar to LY2109761, the peptide antagonist significantly reduced HS FPCL contraction compared with the non-treated group with significant differences in surface area at 48 h (0.71 ± 0.06 cm(2) versus 0.51 ± 0.06 cm(2), p < 0.05) and at 72 h (0.65 ± 0.02 cm(2) versus 0.42 ± 0.01 cm(2), p < 0.05).
  
  
  CONCLUSIONS
  The TGF-β antagonist peptide may serve as an important drug for HS prevention and reduction given the obvious benefits of good biosafety, low cost, and easy manufacture and delivery.
authors.affiliation: a Department of Plastic and Reconstructive Surgery , Shanghai Key Laboratory of Tissue Engineering, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine , Shanghai , PR China and.
authors.forename: Xiuxia
authors.initials: X
authors.lastname: Wang
authors.affiliation: a Department of Plastic and Reconstructive Surgery , Shanghai Key Laboratory of Tissue Engineering, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine , Shanghai , PR China and.
authors.forename: Zhen
authors.initials: Z
authors.lastname: Gao
authors.affiliation: a Department of Plastic and Reconstructive Surgery , Shanghai Key Laboratory of Tissue Engineering, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine , Shanghai , PR China and.
authors.forename: Xiaoli
authors.initials: X
authors.lastname: Wu
authors.affiliation: a Department of Plastic and Reconstructive Surgery , Shanghai Key Laboratory of Tissue Engineering, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine , Shanghai , PR China and.|b National Tissue Engineering Center of China , Shanghai , PR China.
authors.forename: Wenjie
authors.initials: W
authors.lastname: Zhang
authors.affiliation: a Department of Plastic and Reconstructive Surgery , Shanghai Key Laboratory of Tissue Engineering, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine , Shanghai , PR China and.|b National Tissue Engineering Center of China , Shanghai , PR China.
authors.forename: Guangdong
authors.initials: G
authors.lastname: Zhou
authors.affiliation: a Department of Plastic and Reconstructive Surgery , Shanghai Key Laboratory of Tissue Engineering, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine , Shanghai , PR China and.|b National Tissue Engineering Center of China , Shanghai , PR China.
authors.forename: Wei
authors.initials: W
authors.lastname: Liu
mesh_terms: D000328:Adult; D002465:Cell Movement / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D017439:Cicatrix, Hypertrophic / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D005260:Female; D024022:Fibrillar Collagens / Q000235:genetics / Q000378:metabolism; D005347:Fibroblasts / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D005353:Fibronectins / Q000235:genetics / Q000378:metabolism; D005355:Fibrosis; D005786:Gene Expression Regulation; D006801:Humans; D008297:Male; D008875:Middle Aged; D010455:Peptides / Q000494:pharmacology*; D010641:Phenotype; D011720:Pyrazoles / Q000494:pharmacology; D011758:Pyrroles / Q000494:pharmacology; D018125:Receptors, Transforming Growth Factor beta / Q000037:antagonists & inhibitors / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D012867:Skin / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D013997:Time Factors; D053773:Transforming Growth Factor beta1 / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism; D055815:Young Adult
chemical_list: D024022:Fibrillar Collagens; D005353:Fibronectins; C530108:LY2109761; D010455:Peptides; D011720:Pyrazoles; D011758:Pyrroles; D018125:Receptors, Transforming Growth Factor beta; C508960:TGFB1 protein, human; D053773:Transforming Growth Factor beta1
keywords: Cell migration; cell proliferation; matrix production; therapeutic potential