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Amnion membranes support wound granulation in a delayed murine excisional wound model

Chronic or delayed healing wounds constitute an ever‐increasing burden on healthcare providers and patients alike. Thus, therapeutic modalities that are tailored to particular deficiencies in the delayed wound healing response are of critical importance to improve clinical outcomes. Human amnion‐der...

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Autores principales: Dolivo, David, Xie, Ping, Sun, Lauren, Hou, Chun, Phipps, Abigail, Mustoe, Thomas A., Hong, Seok Jong, Galiano, Robert D.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10107106/
https://www.ncbi.nlm.nih.gov/pubmed/36414819
http://dx.doi.org/10.1111/1440-1681.13739
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author Dolivo, David
Xie, Ping
Sun, Lauren
Hou, Chun
Phipps, Abigail
Mustoe, Thomas A.
Hong, Seok Jong
Galiano, Robert D.
author_facet Dolivo, David
Xie, Ping
Sun, Lauren
Hou, Chun
Phipps, Abigail
Mustoe, Thomas A.
Hong, Seok Jong
Galiano, Robert D.
author_sort Dolivo, David
collection PubMed
description Chronic or delayed healing wounds constitute an ever‐increasing burden on healthcare providers and patients alike. Thus, therapeutic modalities that are tailored to particular deficiencies in the delayed wound healing response are of critical importance to improve clinical outcomes. Human amnion‐derived viable and devitalized allografts have demonstrated clinical efficacy in promoting the closure of delayed healing wounds, but the mechanisms responsible for this efficacy and the specific wound healing processes modulated by these tissues are not fully understood. Here, we utilized a diabetic murine excisional wound model in which healing is driven by granulation and re‐epithelialization, and we applied viable (vHAMA) or devitalized (dHAMA) amnion‐derived allografts to the wound bed in order to determine their effects on wound healing processes. Compared to control wounds that were allowed to heal in the absence of treatment, wounds to which vHAMA or dHAMA were applied demonstrated enhanced deposition of granulation tissue accompanied by increased cellular proliferation and increased de novo angiogenesis, while vHAMA‐treated wounds also demonstrated accelerated re‐epithelialization. Taken together, these data suggest that both vHAMA and dHAMA facilitate wound healing through promoting processes critical to granulation tissue formation. Further understanding of the cellular and tissue mechanisms underlying the effects of tissue‐derived matrices on wound healing will enable tailored prescription of their use in order to maximize clinical benefit.
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spelling pubmed-101071062023-04-18 Amnion membranes support wound granulation in a delayed murine excisional wound model Dolivo, David Xie, Ping Sun, Lauren Hou, Chun Phipps, Abigail Mustoe, Thomas A. Hong, Seok Jong Galiano, Robert D. Clin Exp Pharmacol Physiol Original Articles Chronic or delayed healing wounds constitute an ever‐increasing burden on healthcare providers and patients alike. Thus, therapeutic modalities that are tailored to particular deficiencies in the delayed wound healing response are of critical importance to improve clinical outcomes. Human amnion‐derived viable and devitalized allografts have demonstrated clinical efficacy in promoting the closure of delayed healing wounds, but the mechanisms responsible for this efficacy and the specific wound healing processes modulated by these tissues are not fully understood. Here, we utilized a diabetic murine excisional wound model in which healing is driven by granulation and re‐epithelialization, and we applied viable (vHAMA) or devitalized (dHAMA) amnion‐derived allografts to the wound bed in order to determine their effects on wound healing processes. Compared to control wounds that were allowed to heal in the absence of treatment, wounds to which vHAMA or dHAMA were applied demonstrated enhanced deposition of granulation tissue accompanied by increased cellular proliferation and increased de novo angiogenesis, while vHAMA‐treated wounds also demonstrated accelerated re‐epithelialization. Taken together, these data suggest that both vHAMA and dHAMA facilitate wound healing through promoting processes critical to granulation tissue formation. Further understanding of the cellular and tissue mechanisms underlying the effects of tissue‐derived matrices on wound healing will enable tailored prescription of their use in order to maximize clinical benefit. John Wiley and Sons Inc. 2022-12-04 2023-03 /pmc/articles/PMC10107106/ /pubmed/36414819 http://dx.doi.org/10.1111/1440-1681.13739 Text en © 2022 The Authors. Clinical and Experimental Pharmacology and Physiology published by John Wiley & Sons Australia, Ltd. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Original Articles
Dolivo, David
Xie, Ping
Sun, Lauren
Hou, Chun
Phipps, Abigail
Mustoe, Thomas A.
Hong, Seok Jong
Galiano, Robert D.
Amnion membranes support wound granulation in a delayed murine excisional wound model
title Amnion membranes support wound granulation in a delayed murine excisional wound model
title_full Amnion membranes support wound granulation in a delayed murine excisional wound model
title_fullStr Amnion membranes support wound granulation in a delayed murine excisional wound model
title_full_unstemmed Amnion membranes support wound granulation in a delayed murine excisional wound model
title_short Amnion membranes support wound granulation in a delayed murine excisional wound model
title_sort amnion membranes support wound granulation in a delayed murine excisional wound model
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10107106/
https://www.ncbi.nlm.nih.gov/pubmed/36414819
http://dx.doi.org/10.1111/1440-1681.13739
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