The role of mouse mast cell proteases in the proliferative phase of wound healing in microdeformational wound therapy

J Succar, J Douaiher, L Lancerotto, Q Li… - Plastic and …, 2014 - journals.lww.com
J Succar, J Douaiher, L Lancerotto, Q Li, R Yamaguchi, G Younan, G Pejler, DP Orgill
Plastic and reconstructive surgery, 2014journals.lww.com
Background: Stored in the secretory granules of cutaneous mouse mast cells are mouse
mast cell proteases (mMCP-4,-5, and-6). Using transgenic mouse lines that lacked these
enzymes, it was shown that mMCP-4 and mMCP-5 modulate the outcome of burn-induced
skin injury. Whether or not these proteases also play a role in the repair of surgically
damaged skin, with or without microdeformational wound therapy, remains to be
determined. Methods: Wild-type C57BL/6 mice and transgenic C57BL/6 mouse lines lacking …
Abstract
Background:
Stored in the secretory granules of cutaneous mouse mast cells are mouse mast cell proteases (mMCP-4,-5, and-6). Using transgenic mouse lines that lacked these enzymes, it was shown that mMCP-4 and mMCP-5 modulate the outcome of burn-induced skin injury. Whether or not these proteases also play a role in the repair of surgically damaged skin, with or without microdeformational wound therapy, remains to be determined.
Methods:
Wild-type C57BL/6 mice and transgenic C57BL/6 mouse lines lacking mMCP-4,-5, or-6 were subjected to surgical wounding of their skin. Wounds were splinted with a stabilizing patch, and the mice received either microdeformational wound therapy (n= 5) or occlusive dressing (n= 5) for 7 days. Wound healing parameters were assessed in the proliferative phase.
Results:
Cell proliferation in the wounded wild-type mice receiving microdeformational wound therapy was 60±3 percent. Cell proliferation was only 35±5 percent, 25±5 percent, and 45±4 percent for the treated mMCP-4–, mMCP-5–, and mMCP-6–null mice, respectively (p= 0.005). Blood vessel sprouting was higher in the control mice with microdeformational wound therapy (170±40 vessels/high-power field) compared with mouse mast cell protease 6–null mice with microdeformational wound therapy (70±20 vessels/high-power field; p= 0.005), and higher in the control mice with occlusive dressing (110±30 vessels/high-power field) compared with mMCP-4–null mice with occlusive dressing (50±20 vessels/high-power field; p= 0.01). Qualitatively, the granulation tissue of all the protease-deficient groups receiving microdeformational wound therapy was disrupted.
Conclusion:
Results suggest that mouse mast cell proteases 4, 5, and 6 are mediators of the critical role mast cells play in microdeformational wound therapy in the proliferative phase of healing.
Lippincott Williams & Wilkins