Graft–Host Interaction and Its Effect on Wound Repair Using Mouse Models
Autologous skin grafting has been commonly used in clinics for decades to close large wounds, yet the cellular and molecular interactions between the wound bed and the graft that mediates the wound repair are not fully understood. The aim of this study was to better understand the molecular changes...
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Published in | International journal of molecular sciences Vol. 24; no. 22; p. 16277 |
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Abstract | Autologous skin grafting has been commonly used in clinics for decades to close large wounds, yet the cellular and molecular interactions between the wound bed and the graft that mediates the wound repair are not fully understood. The aim of this study was to better understand the molecular changes in the wound triggered by autologous and synthetic grafting. Defining the wound changes at the molecular level during grafting sets the basis to test other engineered skin grafts by design. In this study, a full-thickness skin graft (SKH-1 hairless) mouse model was established. An autologous full-thickness skin graft (FTSG) or an acellular fully synthetic Biodegradable Temporising Matrix (BTM) was grafted. The wound bed/grafts were analysed at histological, RNA, and protein levels during the inflammation (day 1), proliferation (day 5), and remodelling (day 21) phases of wound repair. The results showed that in this mouse model, similar to others, inflammatory marker levels, including Il-6, Cxcl-1, and Cxcl-5/6, were raised within a day post-wounding. Autologous grafting reduced the expression of these inflammatory markers. This was different from the wounds grafted with synthetic dermal grafts, in which Cxcl-1 and Cxcl-5/6 remained significantly high up to 21 days post-grafting. Autologous skin grafting reduced wound contraction compared to wounds that were left to spontaneously repair. Synthetic grafts contracted significantly more than FTSG by day 21. The observed wound contraction in synthetic grafts was most likely mediated at least partly by myofibroblasts. It is possible that high TGF-β1 levels in days 1–21 were the driving force behind myofibroblast abundance in synthetic grafts, although no evidence of TGF-β1-mediated Connective Tissue Growth Factor (CTGF) upregulation was observed. |
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AbstractList | Autologous skin grafting has been commonly used in clinics for decades to close large wounds, yet the cellular and molecular interactions between the wound bed and the graft that mediates the wound repair are not fully understood. The aim of this study was to better understand the molecular changes in the wound triggered by autologous and synthetic grafting. Defining the wound changes at the molecular level during grafting sets the basis to test other engineered skin grafts by design. In this study, a full-thickness skin graft (SKH-1 hairless) mouse model was established. An autologous full-thickness skin graft (FTSG) or an acellular fully synthetic Biodegradable Temporising Matrix (BTM) was grafted. The wound bed/grafts were analysed at histological, RNA, and protein levels during the inflammation (day 1), proliferation (day 5), and remodelling (day 21) phases of wound repair. The results showed that in this mouse model, similar to others, inflammatory marker levels, including Il-6, Cxcl-1, and Cxcl-5/6, were raised within a day post-wounding. Autologous grafting reduced the expression of these inflammatory markers. This was different from the wounds grafted with synthetic dermal grafts, in which Cxcl-1 and Cxcl-5/6 remained significantly high up to 21 days post-grafting. Autologous skin grafting reduced wound contraction compared to wounds that were left to spontaneously repair. Synthetic grafts contracted significantly more than FTSG by day 21. The observed wound contraction in synthetic grafts was most likely mediated at least partly by myofibroblasts. It is possible that high TGF-β1 levels in days 1–21 were the driving force behind myofibroblast abundance in synthetic grafts, although no evidence of TGF-β1-mediated Connective Tissue Growth Factor (CTGF) upregulation was observed. |
Audience | Academic |
Author | Arellano, Carlos Luis Lo, Cheng Hean Akbarzadeh, Shiva Peter, Karlheinz Cleland, Heather Garcia, Nicole Yung-Chih, Chen Rahman, Md Mostafizur Banakh, Ilia |
Author_xml | – sequence: 1 fullname: Garcia, Nicole – sequence: 2 fullname: Rahman, Md Mostafizur – sequence: 3 fullname: Arellano, Carlos Luis – sequence: 4 fullname: Banakh, Ilia – sequence: 5 fullname: Yung-Chih, Chen – sequence: 6 fullname: Peter, Karlheinz – sequence: 7 fullname: Cleland, Heather – sequence: 8 fullname: Lo, Cheng Hean – sequence: 9 fullname: Akbarzadeh, Shiva |
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SubjectTerms | Analysis Angiogenesis Care and treatment Chemokines Collagen Cytokines Fibroblasts IL-6 Inflammation Insulin-like growth factors myofibroblast Plastic surgery RNA Scars Scientific equipment and supplies industry Skin Skin & tissue grafts skin grafting TGF-β1 Transforming growth factors Tumor necrosis factor-TNF Vascular endothelial growth factor Wound healing wound repair Wounds and injuries |
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Title | Graft–Host Interaction and Its Effect on Wound Repair Using Mouse Models |
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