title: Botulinum Toxin Type A Inhibits α-Smooth Muscle Actin and Myosin II Expression in Fibroblasts Derived From Scar Contracture.
abstract: BACKGROUND
  Scar contracture (SC) is one of the most common complications resulting from major burn injuries. Numerous treatments are currently available but they do not always yield excellent therapeutic results. Recent reports suggest that botulinum toxin type A (BTXA) is effective at reducing SC clinically, but the molecular mechanism for this action is unknown. α-Smooth muscle actin (α-SMA) and myosin II are the main components of stress fibers, which are the contractile structures of fibroblasts. The effects of BTXA on α-SMA and myosin II in SC are still unknown. This study aimed to explore the effect of BTXA on α-SMA and myosin II expression in fibroblasts derived from SC and to elucidate its actual mechanism further.
  
  
  METHODS
  Fibroblasts were isolated from tissue specimens of SC. Fibroblasts were cultured in Dulbecco modified Eagle medium with different concentrations of BTXA and their proliferation was analyzed through the tetrazolium-based colorimetric method at 1, 4, and 7 days. Proteins of α-SMA and myosin II were checked using Western blot in fibroblasts treated with different concentrations of BTXA at 1, 4, and 7 days.
  
  
  RESULTS
  Fibroblasts without BTXA treatment had a higher proliferation than that in other groups, which indicated that the proliferation of fibroblasts was significantly inhibited by BTXA (P < 0.05). Proteins of α-SMA and myosin II between fibroblasts with BTXA and fibroblasts without BTXA are statistically significant (P < 0.05).
  
  
  CONCLUSIONS
  These results suggest that BTXA effectively inhibited the growth of fibroblasts derived from SC and reduced the expression of α-SMA and myosin II, which provided theoretical support for the application of BTXA to control SC.
authors.affiliation: From the *Department of Burn and Plastic Surgery, the First Affiliated Hospital of Chinese PLA General Hospital; †Chinese PLA Medical School; and ‡Wound Healing and Cell Biology Laboratory, Burns Institute, the First Affiliated Hospital of Chinese PLA General Hospital, Beijing, People's Republic of China.
authors.forename: Minliang
authors.initials: M
authors.lastname: Chen
authors.forename: Tongtong
authors.initials: T
authors.lastname: Yan
authors.forename: Kui
authors.initials: K
authors.lastname: Ma
authors.forename: Linying
authors.initials: L
authors.lastname: Lai
authors.forename: Chang
authors.initials: C
authors.lastname: Liu
authors.forename: Liming
authors.initials: L
authors.lastname: Liang
authors.forename: Xiaobing
authors.initials: X
authors.lastname: Fu
mesh_terms: D000199:Actins / Q000037:antagonists & inhibitors*; D015415:Biomarkers / Q000378:metabolism; D019274:Botulinum Toxins, Type A / Q000494:pharmacology* / Q000627:therapeutic use; D002056:Burns / Q000150:complications; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D002921:Cicatrix / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism; D003286:Contracture / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism; D003879:Dermatologic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D005347:Fibroblasts / Q000187:drug effects* / Q000378:metabolism; D006801:Humans; D024462:Myosin Type II / Q000037:antagonists & inhibitors*
chemical_list: C541116:ACTA2 protein, human; D000199:Actins; D015415:Biomarkers; D003879:Dermatologic Agents; D019274:Botulinum Toxins, Type A; D024462:Myosin Type II