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Integration of Scaffolds into Full‐Thickness Skin Wounds: The Connexin Response
Author(s) -
Gilmartin Daniel J.,
Alexaline Maia M.,
Thrasivoulou Chris,
Phillips Anthony R. J.,
Jayasinghe Suwan N.,
Becker David L.
Publication year - 2013
Publication title -
advanced healthcare materials
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.288
H-Index - 90
eISSN - 2192-2659
pISSN - 2192-2640
DOI - 10.1002/adhm.201200357
Subject(s) - wound healing , connexin , epidermis (zoology) , biocompatibility , scaffold , inflammation , gap junction , microbiology and biotechnology , materials science , biomedical engineering , medicine , anatomy , immunology , biology , intracellular , metallurgy
Scaffolds have been reported to promote healing of hard‐to‐heal wounds such as burns and chronic ulcers. However, there has been little investigation into the cell biology of wound edge tissues in response to the scaffolds. Here, we assess the impact of collagen scaffolds on mouse full‐thickness wound re‐epithelialisation during the first 5 days of healing. We find that scaffolds impede wound re‐epithelialisation, inducing a bulbous thickening of the wound edge epidermis as opposed to the thin tongue of migratory keratinocytes seen in normal wound healing. Scaffolds also increase the inflammatory response and the numbers of neutrophils in and around the wound. These effects were also produced by scaffolds made of alginate in the form of fibers and microspheres, but not as an alginate hydrogel. In addition, we find the gap junction protein connexin 43, which normally down‐regulates at the wound edge during re‐epithelialisation, to be up‐regulated in the bulbous epidermal wound edge. Incorporation of connexin 43 antisense oligodeoxynucleotides into the scaffold can be performed to reduce inflammation whilst promoting scaffold biocompatibility.