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      A Translational Animal Model for Scar Compression Therapy Using an Automated Pressure Delivery System

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          Abstract

          Background: Pressure therapy has been used to prevent and treat hypertrophic scars following cutaneous injury despite the limited understanding of its mechanism of action and lack of established animal model to optimize its usage. Objectives: The aim of this work was to test and characterize a novel automated pressure delivery system designed to deliver steady and controllable pressure in a red Duroc swine hypertrophic scar model. Methods: Excisional wounds were created by dermatome on 6 red Duroc pigs and allowed to scar while assessed weekly via gross visual inspection, laser Doppler imaging, and biopsy. A portable novel automated pressure delivery system was mounted on developing scars ( n = 6) for 2 weeks. Results: The device maintained a pressure range of 30 ± 4 mm Hg for more than 90% of the 2-week treatment period. Pressure readings outside this designated range were attributed to normal animal behavior and responses to healing progression. Gross scar examination by the Vancouver Scar Scale showed significant and sustained (>4 weeks) improvement in pressure-treated scars ( P < .05). Histological examination of pressure-treated scars showed a significant decrease in dermal thickness compared with other groups ( P < .05). Pressure-treated scars also showed increased perfusion by laser Doppler imaging during the treatment period compared with sham-treated and untreated scars ( P < .05). Cellular quantification showed differential changes among treatment groups. Conclusion: These results illustrate the applications of this technology in hypertrophic scar Duroc swine model and the evaluation and optimization of pressure therapy in wound-healing and hypertrophic scar management.

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          Hypoxic tumor cell modulates its microenvironment to enhance angiogenic and metastatic potential by secretion of proteins and exosomes.

          Jung Eun Park, Hon Sen Tan, Arnab Datta … (2010)
          Under hypoxia, tumor cells produce a secretion that modulates their microenvironment to facilitate tumor angiogenesis and metastasis. Here, we observed that hypoxic or reoxygenated A431 carcinoma cells exhibited enhanced angiogenic and metastatic potential such as reduced cell-cell and cell-extracellular matrix adhesion, increased invasiveness, and production of a secretion with increased chorioallantoic membrane angiogenic activity. Consistent with these observations, quantitative proteomics revealed that under hypoxia the tumor cells secreted proteins involved in angiogenesis, focal adhesion, extracellular matrix-receptor interaction, and immune cell recruitment. Unexpectedly, the secreted proteins were predominantly cytoplasmic and membrane proteins. Ultracentrifugation at 100,000 x g precipitated 54% of the secreted proteins and enriched for many exosome-associated proteins such as the tetraspanins and Alix and also proteins with the potential to facilitate angiogenesis and metastasis. Two tetraspanins, CD9 and CD81, co-immunoprecipitated. Together, these data suggested that tumor cells secrete proteins and exosomes with the potential to modulate their microenvironment and facilitate angiogenesis and metastasis.
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            Apoptosis mediates the decrease in cellularity during the transition between granulation tissue and scar.

            A Desmoulière, M Redard, I Darby … (1995)
            Granulation tissue formation and contraction is an important step of second intention wound healing. Granulation tissue develops from the connective tissue surrounding the damaged or missing area and its cellular components are mainly small vessel and inflammatory cells as well as fibroblasts and myofibroblasts. As the wound closes and evolves into a scar, there is an important decrease in cellularity; in particular myofibroblasts disappear. The question arises as to which process is responsible for this cellular loss. During a previous investigation on the expression of alpha-smooth muscle actin in myofibroblasts (Darby I, Skalli O, Gabbiani G, Lab Invest, 1990, 63:21-29), we have observed that in late phases of wound healing, many myofibroblasts show changes compatible with apoptosis and suggested that this type of cell death could be responsible for the disappearance of myofibroblasts. We have now tested this hypothesis by means of morphometry at the electron microscopic level and by in situ end labeling of fragmented DNA. Our results indicate that the number of myofibroblastic and vascular cells undergoing apoptosis increases as the wound closes and support the assumption that this is the mechanism of granulation tissue evolution into a scar. The regulation of apoptotic phenomena during wound healing may be important in scar establishment and development of pathological scarring.
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              Mechanical load initiates hypertrophic scar formation through decreased cellular apoptosis.

              Shahram Aarabi, Yubin Shi, Charles W. Holmes … (2007)
              Hypertrophic scars occur following cutaneous wounding and result in severe functional and esthetic defects. The pathophysiology of this process remains unknown. Here, we demonstrate for the first time that mechanical stress applied to a healing wound is sufficient to produce hypertrophic scars in mice. The resulting scars are histopathologically identical to human hypertrophic scars and persist for more than six months following a brief (one-week) period of augmented mechanical stress during the proliferative phase of wound healing. Resulting scars are structurally identical to human hypertrophic scars and showed dramatic increases in volume (20-fold) and cellular density (20-fold). The increased cellularity is accompanied by a four-fold decrease in cellular apoptosis and increased activation of the prosurvival marker Akt. To clarify the importance of apoptosis in hypertrophic scar formation, we examine the effects of mechanical loading on cutaneous wounds of animals with altered pathways of cellular apoptosis. In p53-null mice, with down-regulated cellular apoptosis, we observe significantly greater scar hypertrophy and cellular density. Conversely, scar hypertrophy and cellular density are significantly reduced in proapoptotic BclII-null mice. We conclude that mechanical loading early in the proliferative phase of wound healing produces hypertrophic scars by inhibiting cellular apoptosis through an Akt-dependent mechanism.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Eplasty
                Journal ID (iso-abbrev): Eplasty
                Journal ID (publisher-id): ePlasty
                Title: Eplasty
                Publisher: Open Science Company, LLC
                ISSN (Electronic): 1937-5719
                Publication date Collection: 2015
                Publication date (Electronic): 2 July 2015
                Volume: 15
                Electronic Location Identifier: e29
                Affiliations
                [1] aFirefighters’ Burn and Surgical Research Laboratory, MedStar Health Research Institute, Washington, DC
                [2] bThe Burn Center, Department of Surgery, MedStar Washington Hospital Center, Washington, DC
                [3] cDepartment of Biomedical Engineering, Florida International University, Miami
                Author notes

                Drs Alkhalil and Tejiram contributed equally to manuscript preparation and seek first authorship.

                This work was funded by the NIH grant no. 1R15EB013439.

                Article
                Publisher ID: 29
                PMC ID: 4492193
                SO-VID: 0e286e2f-b87b-401d-b288-d2a0fd9d6a16
                Copyright © Copyright © 2015 The Author(s)
                License:

                This is an open-access article whereby the authors retain copyright of the work. The article is distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Categories
                Subject: Journal Article

                ScienceOpen disciplines: Surgery
                Keywords: wound,pressure therapy,scar,animal model,red duroc pig
                Data availability:
                ScienceOpen disciplines: Surgery
                Keywords: wound, pressure therapy, scar, animal model, red duroc pig

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