Chinese Journal of Tissue Engineering Research ›› 2012, Vol. 16 ›› Issue (2): 235-238.doi: 10.3969/j.issn.1673-8225.2012.02.010

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Effects of mitomycin C on apoptosis of hypertrophic scar fibroblasts

Wu Xiao-ming, Sun Kui, Zhang Hong-xia, Sun Xi-ping, Geng Qi-ying, Li Shu-song   

  1. Department of Burnand Plastic Surgery,Affiliated Hospital ofChengde MedicalUniversity, Chengde067000, HebeiProvince, China
  • Received:2011-10-10 Revised:2011-12-09 Online:2012-01-08 Published:2012-01-08
  • About author:Wu Xiao-ming★,Master, Attendingphysician,Department of Burnand Plastic Surgery,Affiliated Hospital ofChengde MedicalUniversity, Chengde067000, HebeiProvince, China sszxwk@sohu.com Sun Kui, Master,Attending physician,Department of Burnand Plastic Surgery,Affiliated Hospital ofChengde MedicalUniversity, Chengde067000, HebeiProvince, China Wu Xiao-ming andSun Kui contributedequally to this study.

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Abstract:

BACKGROUND: Mitomycin C has been gradually used in hyperplastic scar therapy. But the molecular mechanism underlyingthe effects of mitomycin C on hyperplastic scar via cell apoptosis is reported few.
OBJECTIVE: To explore the effects of mitomycin C on fibroblasts apoptosis in hypertrophic scar.
METHODS: Hypertrophic scar fibroblasts were cultured in vitro with five different concentrations of mitomycin C (2.5, 12.5, 50,100, 200 mg/L). Cell cycle distribution and apoptosis of fibroblasts were detected by Annexin V-PI, and the protein expressionlevels of Bax and Bcl-2 in fibroblasts were detected with Western blotting.
RESULTS AND CONCLUSION: Mitomycin C blocked the growth of hyperplastic scar fibroblasts in G0/G1 period, and inducedapoptosis of hyperplastic scar fibroblasts in an obvious concentration-dependent manner. Bax protein expression levelsincreased and Bcl-2 protein expression levels decreased in hyperplastic scar fibroblasts after treated with 2.5-200 mg/Lmitomycin C for 24 hours (P < 0.05). These findings indicate that mitomycin C has the possibility to promote fibroblasts apoptosisthrough increasing Bax expression and decreasing Bcl-2 expression in hyperplastic scar fibroblasts