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Matrix metalloproteinase inhibition delays wound healing and blocks the latent transforming growth

Ursula Mirastschijski1, Reinhild Schnabel, Juliane Claes

  • 1Department of Plastic, Hand and Reconstructive Surgery, Hannover Medical School, Hannover, Germany.

Wound Repair and Regeneration : Official Publication of the Wound Healing Society [And] the European Tissue Repair Society
|April 23, 2010
PubMed

Insights

The broad-spectrum matrix metalloproteinase (MMP) inhibitor BB-94 delays wound healing by inhibiting myofibroblast formation and transforming growth factor-beta1 (TGF-beta1) activation. Increased MMP-9 levels may overcome BB-94

Area of Science:

  • Wound Healing Research
  • Dermatology
  • Pharmacology

Background:

  • Wound contraction regulation is vital for healing and pathological contractures.
  • Matrix metalloproteinases (MMPs) are essential for normal wound healing processes.
  • Transforming growth factor-beta1 (TGF-beta1) plays a role in myofibroblast formation and function.

Purpose of the Study:

  • To investigate the topical effects of the MMP inhibitor BB-94 on wound healing in rats.
  • To assess BB-94's impact on myofibroblast development and TGF-beta1 promotion.
  • To elucidate the mechanisms underlying BB-94's influence on wound contraction.

Main Methods:

  • Application of broad-spectrum MMP inhibitor BB-94 to full-thickness skin excisional wounds in rats.
  • Evaluation of wound contraction, myofibroblast formation, cell proliferation, angiogenesis, and epithelialization.
  • Measurement of latent and active MMP-9 levels and TGF-beta1 activation.

Main Results:

  • BB-94 significantly delayed wound contraction and associated healing parameters.
  • BB-94 inhibited myofibroblast formation, stromal cell proliferation, blood vessel formation, and epithelial coverage.
  • BB-94 treatment led to a dramatic increase in both latent and active MMP-9 levels.
  • BB-94 inhibited the promotion of myofibroblast formation and function by latent TGF-beta1.

Conclusions:

  • BB-94 delays wound closure via a dual mechanism: inhibiting keratinocyte migration and subsequent myofibroblast formation, and blocking latent TGF-beta1 activation.
  • Elevated MMP-9 levels may counteract BB-94's inhibitory effects, leading to delayed rather than complete inhibition of wound healing.
  • These findings highlight the complex role of MMPs and TGF-beta1 in wound healing and the potential of MMP inhibitors in modulating these processes.

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