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Plast Reconstr Surg. 2014 Sep;134(3):459-67. doi: 10.1097/PRS.0000000000000432.

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

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Lexington, Ky.; Baltimore, Md.; Padova, Italy; Shanghai, People's Republic of China; Ibaraki, Japan; Falls Church, Va.; Uppsala, Sweden; and Boston, Mass. From the Department of General Surgery, University of Kentucky; Department of General Surgery, Johns Hopkins University; Department of Plastic Surgery, Padova University; Department of Plastic Surgery, Changzheng Hospital; Department of Surgery, Mito Chuo Hospital; Department of General Surgery, Inova Fairfax Hospital; Department of Anatomy, Physiology, and Biochemistry, Swedish University of Agricultural Sciences; and Division of Plastic Surgery, Brigham and Women's Hospital and Harvard Medical School.



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.


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.


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.


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.

[Indexed for MEDLINE]

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