Effects of Mitomycin-C on Normal Dermal Fibroblasts

Authors

  • Theodore Chen MD,

    1. Wound Healing and Tissue Engineering Laboratory, Department of Otolaryngology—Head and Neck Surgery, Stanford University Medical Center, Stanford, California, U.S.A.
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  • Shaun S. Kunnavatana BA,

    1. Wound Healing and Tissue Engineering Laboratory, Department of Otolaryngology—Head and Neck Surgery, Stanford University Medical Center, Stanford, California, U.S.A.
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  • R James Koch MD, MS

    Corresponding author
    1. Wound Healing and Tissue Engineering Laboratory, Department of Otolaryngology—Head and Neck Surgery, Stanford University Medical Center, Stanford, California, U.S.A.
    • Dr. R. James Koch, Department of Otolaryngology–Head and Neck Surgery, 801 Welch Road, Stanford, CA 94305-5739
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  • Western Section Meeting of the Triological Society, February 4, 2005, Las Vegas, Nevada, U.S.A.

    The authors do not have any financial, commercial, or proprietary interest in the products or companies used. Likewise, they have not received payments as consultants, reviewers, or evaluators of these products or companies.

Abstract

Objectives: To evaluate the effects of mitomycin-C on the growth and autocrine growth factor production of human dermal fibroblasts from the face.

Study Design: In vitro study using normal adult dermal fibroblast cell lines in a serum-free model.

Methods: Cell cultures were exposed to 4 mg/mL, 0.4 mg/mL, 0.04 mg/mL, 0.004 mg/mL, and 0.0004 mg/mL concentrations of mitomycin-C solution. Cell counts were performed, and the cell-free supernatants were collected at 0, 1, 3, and 5 days after the initial exposure. Population doubling times were calculated and supernatants were quantitatively assayed for basic fibroblast growth factor (bFGF) and transforming growth factor (TGF)-β1.

Results: Continuous exposure to mitomycin-C caused fibroblast cell death by day 7 at all tested concentrations. A 4 minute exposure to mitomycin-C at 4 mg/mL caused rapid fibroblast cell death. A 4-minute exposure to mitomycin-C at either 0.4 mg/mL or 0.04 mg/mL resulted in decreased fibroblast proliferation. A 4 minute exposure to mitomycin-C at 0.4 mg/mL resulted in a marked increase in the production of both bFGF and TGF-β1.

Conclusions: A clinically ideal concentration of mitomycin-C would slow fibroblast proliferation yet not cause cell death to allow for a wound healing response. Mitomycin-C 0.4 mg/mL for 4 minutes satisfies the above criteria in vitro.

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