title: Effects of botulinum toxin type A on expression of genes in keloid fibroblasts.
abstract: BACKGROUND
  Invasive growth of fibroblast cells, which is regulated by multiple biological factors, is the key event in the pathophysiology of keloid scars. Recent studies have suggested that botulinum toxin type A (BoNT-A) could inhibit invasive growth of keloids. However, the molecular mechanisms are unknown.
  
  
  OBJECTIVE
  The authors explore the effect of BoNT-A on the expression of genes relevant to invasive growth in keloid fibroblasts.
  
  
  METHODS
  With 112 genes that were relevant to invasive growth, the authors utilized microarray analysis to study messenger RNA expression profiles in keloid fibroblasts treated with BoNT-A. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to confirm the microarray results.
  
  
  RESULTS
  Analyses from microarray and qRT-PCR revealed that the S100A4 gene was upregulated and that the TGF-β1, VEGF, MMP-1, and PDGFA genes were downregulated in fibroblasts treated with BoNT-A.
  
  
  CONCLUSIONS
  The BoNT-A altered expression levels of S100A4, TGF-β1, VEGF, MMP-1, and PDGFA genes in keloid fibroblasts provide a useful clue for exploring the function of BoNT-A and finding a novel treatment for keloid scarring.
authors.affiliation: Second Affiliated Hospital of the Harbin Medical University, Harbin City, China.
authors.forename: Wang
authors.initials: W
authors.lastname: Xiaoxue
authors.forename: Chen
authors.initials: C
authors.lastname: Xi
authors.forename: Xiao
authors.initials: X
authors.lastname: Zhibo
mesh_terms: D019274:Botulinum Toxins, Type A / Q000494:pharmacology*; D049109:Cell Proliferation / Q000187:drug effects*; D002478:Cells, Cultured; D003879:Dermatologic Agents / Q000494:pharmacology*; D005347:Fibroblasts / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D020869:Gene Expression Profiling / Q000379:methods; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D007627:Keloid / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D020781:Matrix Metalloproteinase 1 / Q000235:genetics; D020411:Oligonucleotide Array Sequence Analysis; D010982:Platelet-Derived Growth Factor / Q000235:genetics; D012333:RNA, Messenger / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction; D000071999:S100 Calcium-Binding Protein A4; D009418:S100 Proteins / Q000235:genetics; D012867:Skin / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D013997:Time Factors; D053773:Transforming Growth Factor beta1 / Q000235:genetics; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics
chemical_list: D003879:Dermatologic Agents; D010982:Platelet-Derived Growth Factor; D012333:RNA, Messenger; D000071999:S100 Calcium-Binding Protein A4; D009418:S100 Proteins; C508960:TGFB1 protein, human; D053773:Transforming Growth Factor beta1; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; C075278:platelet-derived growth factor A; C077591:S100A4 protein, human; D019274:Botulinum Toxins, Type A; C545476:incobotulinumtoxinA; C522360:MMP1 protein, human; D020781:Matrix Metalloproteinase 1
keywords: botulinum toxin type A; fibroblast; gene expression; invasive growth; keloid; research