期刊
ADVANCES IN WOUND CARE
卷 12, 期 6, 页码 301-315出版社
MARY ANN LIEBERT, INC
DOI: 10.1089/wound.2022.0005
关键词
wound healing; chronic wound; diabetes; oxidative stress; angiogenesis; diabetic wound; tissue regeneration; allograft; amniotic membrane
类别
This study investigated the effect of human amniotic membrane (AM) on chronic wound healing using an oxidative stress murine model. The results showed that AM treatment increased vascular density and maturity, promoted leukocyte infiltration and growth factor delivery, and reduced cell death. These findings provide new insights into the mechanisms of action of human AM in chronic wound healing.
Objective: The development of animal models, which adequately replicate the pathophysiology of chronic wounds, has been challenging. In this study, we utilized an oxidative stress (OS) murine model, which was previously developed by our group, to study the effect of a human amniotic membrane (AM) on chronic wound healing.& nbsp;Approach: Forty-five diabetic (genetically obese leptin receptor-deficient mice [db/db]) mice were separated into three groups. Thirty mice received an OS regimen and a 1 - x 1 cm(2) full-thickness excisional dorsal wound. The wounds were either covered with AM and occlusive dressing (db/db(OS)-AM) or occlusive dressing only (db/db(OS)). Fifteen mice did not receive the OS regimen, and were covered with AM and occlusive dressing (db/db-AM). The wounds were photographed, and tissue was harvested at various time points.& nbsp;Results: Vascular density was higher in the AM-treated groups (db/db(OS)-AM: 34 +/-& nbsp;12; db/db-AM: 37 +/- 14; vs. db/db(OS): 19 +/- 9 cluster of differentiation 31 [CD31(+)]/high power field [HPF] photograph; p = 0.04 and p = 0.003). Vessel maturity was lowest in the db/db(OS) group (21% +/-& nbsp;4%; vs. db/db(OS)-AM: 38%& nbsp;+/- 10%, p = 0.004; db/db-AM: 40% +/- 11%, p = 0.0005). Leukocyte infiltration was higher in the AM groups (db/db(OS)-AM: 15 +/-& nbsp;4; db/db-AM: 16 v +/-& nbsp;4 vs. db/db(OS): 8 +/-& nbsp;3 lymphocyte common antigen [CD45(+)]/HPF; p = 0.005 and p = 0.06). AM upregulated various proangiogenic factors, including vascular endothelial growth factor (VEGF), and downregulated genes involved in chronicity, such as osteopontin, as visualized through proteome analysis and western blotting. Cell death was lower in the AM groups (db/db(OS)-AM: 28 +/-& nbsp;10, db/db-AM: 7 +/- 5 vs. db/db(OS): 17% +/-& nbsp;9% Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling [TUNEL+]; p = 0.03 and p < 0.0001).& nbsp;Innovation: This study offers new insight on the mechanisms of action of human AM in chronic wound healing.& nbsp;Conclusion: AM treatment promoted healing in mice with complex chronic wounds. The AM stimulated angiogenesis through upregulation of proangiogenic factors, improving the wound milieu by increasing leukocyte and growth factor delivery and decreasing cell death.
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