The Role of Mouse Mast Cell Proteases in the Proliferative Phase of Wound Healing in Microdeformational Wound Therapy

Succar, Julien; Douaiher, Jeffrey; Lancerotto, Luca; Li, Qiong; Yamaguchi, Ryushiro; Younan, George; Pejler, Gunnar; Orgill, Dennis P.

doi:10.1097/prs.0000000000000432

Cited by 15 publications

(16 citation statements)

References 52 publications

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“…Their dorsum was disinfected with 70% alcohol and marked with standard square template (1.0 cm 2 ). Skin plus panniculus carnosus was excised to create a full-thickness dorsal excisional wound, which was covered with transparent, semiocclusive adhesive polyurethane dressings (Tegaderm; 3M, St. Paul, MN) and changed two times per week (30–32). …”

Section: Methodsmentioning

confidence: 99%

“…Standardized photographs were taken on the day of surgery and on the 3rd, 7th, 10th, and 14th days for 14 days from a standard height. Re-epithelialization and open wound surface were measured as a percentage of the initial wound area as published (30–32). …”

Section: Methodsmentioning

confidence: 99%

“…On days 3, 7, and 10 postsurgery, wounds from seven to eight animals in each group were harvested as previously described (32). …”

Section: Methodsmentioning

confidence: 99%

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Overexpressing IRS1 in Endothelial Cells Enhances Angioblast Differentiation and Wound Healing in Diabetes and Insulin Resistance

et al. 2016

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The effect of enhancing insulin’s actions in endothelial cells (ECs) to improve angiogenesis and wound healing was studied in obesity and diabetes. Insulin receptor substrate 1 (IRS1) was overexpressed in ECs using the VE-cadherin promoter to create ECIRS1 TG mice, which elevated pAkt activation and expressions of vascular endothelial growth factor (VEGF), Flk1, and VE-cadherin in ECs and granulation tissues (GTs) of full-thickness wounds. Open wound and epithelialization rates and angiogenesis significantly improved in normal mice and high fat (HF) diet–induced diabetic mice with hyperinsulinemia in ECIRS1 TG versus wild type (WT), but not in insulin-deficient diabetic mice. Increased angioblasts and EC numbers in GT of ECIRS1 mice were due to proliferation in situ rather than uptake. GT in HF-fed diabetic mice exhibited parallel decreases in insulin and VEGF-induced pAkt and EC numbers by >50% without changes in angioblasts versus WT mice, which were improved in ECIRS1 TG mice on normal chow or HF diet. Thus, HF-induced diabetes impaired angiogenesis by inhibiting insulin signaling in GT to decrease the differentiation of angioblasts to EC, which was normalized by enhancing insulin’s action targeted to EC, a potential target to improve wound healing in diabetes and obesity.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Overexpressing IRS1 in Endothelial Cells Enhances Angioblast Differentiation and Wound Healing in Diabetes and Insulin Resistance

et al. 2016

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“…On days 0, 3, 6, 9, 12, and 15 after surgery, reepithelialization of the wound was monitored macroscopically (assessed on the basis of the absence of redness and fluid exudate), and the wound's open area was digitally photographed. On days 9 and 15 after surgery, wounds from 6 animals in each group were harvested as previously described (58). In another series of experiments, fibroblasts from controls were infected with either adenoviral vectors containing GFP (Ad-GFP) or with WT PKCδ isoforms (Ad-wtPKCδ).…”

Section: Histological and Immunohistochemical Analysesmentioning

confidence: 99%

PKCδ inhibition normalizes the wound-healing capacity of diabetic human fibroblasts

Khamaisi¹,

Katagiri²,

Keenan³

et al. 2016

Journal of Clinical Investigation

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“…By contrast, the role of MCs in skin wound healing is controversial. Whereas some studies indicate that MCs are essential in certain models of wound healing (9)(10)(11)(12), others found that skin wound closure may not be affected by the absence of MCs (13)(14)(15).…”

mentioning

confidence: 99%

Mast cells are critical for controlling the bacterial burden and the healing of infected wounds

Zimmermann

Troeltzsch

Giménez-Rivera

et al. 2019

Proc. Natl. Acad. Sci. U.S.A.

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Skin wound infections are a significant health problem, and antibiotic resistance is on the rise. Mast cells (MCs) have been shown to contribute to host–defense responses in certain bacterial infections, but their role in skin wound superinfection is unknown. We subjected 2 MC-deficient mouse strains to Pseudomonas aeruginosa skin wound infection and found significantly delayed wound closure in infected skin wounds. This delay was associated with impaired bacterial clearance in the absence of MCs. Engraftment of MCs restored both bacterial clearance and wound closure. Bacterial killing was dependent on IL-6 released from MCs, and engraftment with IL-6–deficient MCs failed to control wound infection. Treatment with recombinant IL-6 enhanced bacterial killing and resulted in the control of wound infection and normal wound healing in vivo. Taken together, our results demonstrate a defense mechanism for boosting host innate immune responses, namely effects of MC-derived IL-6 on antimicrobial functions of keratinocytes.

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The Role of Mouse Mast Cell Proteases in the Proliferative Phase of Wound Healing in Microdeformational Wound Therapy

Abstract: Results suggest that mouse mast cell proteases 4, 5, and 6 are mediators of the critical role mast cells play in microdeformational wound therapy in the proliferative phase of healing.

Cited by 15 publications

References 52 publications

Overexpressing IRS1 in Endothelial Cells Enhances Angioblast Differentiation and Wound Healing in Diabetes and Insulin Resistance

Overexpressing IRS1 in Endothelial Cells Enhances Angioblast Differentiation and Wound Healing in Diabetes and Insulin Resistance

PKCδ inhibition normalizes the wound-healing capacity of diabetic human fibroblasts

Mast cells are critical for controlling the bacterial burden and the healing of infected wounds

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