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Combination of stromal cell-derived factor-1 and collagen–glycosaminoglycan scaffold delays contraction and accelerates reepithelialization of dermal wounds in wild-type mice

Authors

  • Aparajita Sarkar MS,

    1. Center for Engineering in Medicine/Surgical Services, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts,
    2. Shriners Hospitals for Children, Boston, Massachusetts,
    3. Department of Mechanical Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts,
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  • Soner Tatlidede MD,

    1. Shriners Hospitals for Children, Boston, Massachusetts,
    2. Division of Plastic Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts,
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  • Saja Sandra Scherer MD,

    1. Division of Plastic Surgery, Brigham & Women's Hospital, Harvard Medical School, Boston, Massachusetts, and
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  • Dennis P. Orgill MD, PhD,

    1. Division of Plastic Surgery, Brigham & Women's Hospital, Harvard Medical School, Boston, Massachusetts, and
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  • François Berthiaume PhD

    1. Center for Engineering in Medicine/Surgical Services, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts,
    2. Shriners Hospitals for Children, Boston, Massachusetts,
    3. Department of Biomedical Engineering, Rutgers University, Piscataway, New Jersey
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Reprint requests:
François Berthiaume, PhD, Rutgers University, 599 Taylor Road, Piscataway, NJ 08854, USA. Tel: +1 732-445-4500;
Fax: +1 732-445-3753;
Email: fberthia@rci.rutgers.edu

ABSTRACT

While dermal substitutes can mitigate scarring and wound contraction, a significant drawback of current dermal replacement technologies is the apparent delay in vascular ingrowth compared with conventional skin grafts. Herein, we examined the effect of the chemokine stromal cell-derived factor-1 (SDF-1) on the performance of a porous collagen–glycosaminoglycan dermal analog in excisional wounds in mice. C57BL/6 mice with 1 cm × 1 cm dorsal full-thickness wounds were covered with a collagen–glycosaminoglycan scaffold, followed by four daily topical applications of 1 μg SDF-1 or phosphate-buffered saline vehicle. Some animals were also pretreated with five daily doses of 300 mg/kg granulocyte colony-stimulating factor. Animals treated with SDF-1 and no granulocyte colony-stimulating factor reepithelialized 36% faster than vehicle controls (16 vs. 25 days), and exhibited less wound contraction on postwounding day 18 (∼35% greater wound area) plus three-fold longer neoepidermis formed than controls. Conversely, granulocyte colony-stimulating factor promoted contraction and no epidermal regeneration. Early (postwounding Day 3) inflammatory cell infiltration in the SDF-1-treated group was 86% less, while the fraction of proliferating cells (positive Ki67 staining) was 32% more, when compared with controls. These results suggest that SDF-1 simultaneously delays contraction and promotes reepithelialization and may improve the wound-healing performance of skin substitutes.

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