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

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Sarkar, Aparajita
Tatlidede, Soner
Scherer, Saja Sandra
Berthiaume, François
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https://doi.org/10.1111/j.1524-475X.2010.00646.xMetadata
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Sarkar, Aparajita, Soner Tatlidede, Saja Sandra Scherer, Dennis P. Orgill, and François Berthiaume. 2010. “Combination of Stromal Cell-Derived Factor-1 and Collagen-Glycosaminoglycan Scaffold Delays Contraction and Accelerates Reepithelialization of Dermal Wounds in Wild-Type Mice.” Wound Repair and Regeneration 19 (1) (December 6): 71–79. doi:10.1111/j.1524-475x.2010.00646.x.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.Other Sources
http://www.ncbi.nlm.nih.gov/pubmed/21134036Terms of Use
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