Mast Cells Contribute to Scar Formation during Fetal Wound Healing

Wulff, Brian C.; Parent, Allison E.; Meleski, Melissa; DiPietro, Luisa A.; Schrementi, Megan E.; Wilgus, Traci A.

doi:10.1038/jid.2011.324

Cited by 157 publications

(138 citation statements)

References 52 publications

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“…The normal wound closure in CreMaster mice that we observed at the macroscopic and histological level is consistent with recent data, which demonstrated that wound closure as assessed macroscopically was not affected in splinted excisional wounds of three different types of mast cell-deficient mice, including Kit W /Kit Wv mice (6). Mast cells had previously been shown to contribute to collagen remodeling after completion of healing (5) and to scar formation during fetal wound healing (36). However, the analysis of 13-d wounds revealed no obvious difference in the area and density of the late granulation tissue/early scar tissue, although more subtle differences in collagen remodeling after completion of wounding cannot be excluded.…”

Section: Discussionmentioning

confidence: 72%

Mast Cells Are Dispensable for Normal and Activin-Promoted Wound Healing and Skin Carcinogenesis

Antsiferova

Martin

Huber

et al. 2013

The Journal of Immunology

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The growth and differentiation factor activin A is a key regulator of tissue repair, inflammation, fibrosis, and tumorigenesis. However, the cellular targets, which mediate the different activin functions, are still largely unknown. In this study, we show that activin increases the number of mature mast cells in mouse skin in vivo. To determine the relevance of this finding for wound healing and skin carcinogenesis, we mated activin transgenic mice with CreMaster mice, which are characterized by Cre recombinase-mediated mast cell eradication. Using single- and double-mutant mice, we show that loss of mast cells neither affected the stimulatory effect of overexpressed activin on granulation tissue formation and reepithelialization of skin wounds nor its protumorigenic activity in a model of chemically induced skin carcinogenesis. Furthermore, mast cell deficiency did not alter wounding-induced inflammation and new tissue formation or chemically induced angiogenesis and tumorigenesis in mice with normal activin levels. These findings reveal that mast cells are not major targets of activin during wound healing and skin cancer development and also argue against nonredundant functions of mast cells in wound healing and skin carcinogenesis in general.

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Section: Discussionmentioning

confidence: 72%

Mast Cells Are Dispensable for Normal and Activin-Promoted Wound Healing and Skin Carcinogenesis

Antsiferova

Martin

Huber

et al. 2013

The Journal of Immunology

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“…[6] Besides, a much larger population is badly in need of scar reduction therapies. [7,8] Although recent research has elucidated many factors and details that contribute to scar formation, [6,[9][10][11] www.advancedsciencenews.com www.advhealthmat.de factor (PDGF), TGF-β, vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), and epidermal growth factor (EGF)). [29,30] Thus, macrophages may either induce tissue destruction (M1) or initiate regeneration (M2).…”

Section: Introductionmentioning

confidence: 99%

Pro‐Regenerative Hydrogel Restores Scarless Skin during Cutaneous Wound Healing

Sun

2017

Adv Healthcare Materials

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The transformation of fibrotic healing process to regenerative one has great potential to fully restore wounded skin. The M2 macrophage phenotype promotes constructive tissue remodeling and instructs tissue repair in a regenerative manner. It is hypothesized that hydrogels that can establish robustness of endogenous cells to regulate M2 phenotype will promote constructive dermal remodeling. Toward this end, a series of dextran‐based bioabsorbable hydrogels are developed and self‐crosslinkable dextran‐isocyanatoethyl methacrylate‐ethylamine (DexIEME) is identified as the potential scaffold. The initial screening study revealed that DexIEME has superior biocompatibility in varying concentrations. Although DexIEME brings about low proinflammatory responses, it promotes M2 macrophage phenotype. Then the optimized hydrogel formulation is tested for acute skin injuries using both murine and porcine models. Preliminary data demonstrated that the innovative DexIEME hydrogel promotes complete skin regeneration with hair regrowth on pre‐existing scars, while untreated scars remain intact. Preclinical studies further demonstrated that the DexIEME hydrogel regenerated perfect skin during deep porcine wound healing. Overall, the approach to investigate immune‐modulated hydrogels yields pro‐regenerative DexIEME hydrogel, which may lead to greater clinical success in treating deep dermal injury and attenuating scar formation.

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“…[34] This suggests that mast cells may also contribute to the foetal arteriogenesis by assisting formation of elastic fibres. In addition to the perivascular area, the mast cell population is clearly enriched in all the elastic tissue/organs including arteries, skin and lung, indicating a universal link between mast cells and elastin.…”

Section: Discussionmentioning

confidence: 99%

Perivascular mast cells promote neointimal elastin deposition and suppress chronic vein graft restenosis in hyperlipidaemic mice

Lawrence

Wadsworth

et al. 2017

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How to cite this article: Wu J, Lawrence C, Wadsworth RM, Kennedy S. Perivascular mast cells promote neointimal elastin deposition and suppress chronic vein graft restenosis in hyperlipidaemic mice. Vessel Plus 2017;1:137-44.Aim: Mast cells are versatile innate immune cells and are reported to promote vascular inflammation and neointimal lesion formation, thereby contributing to the development of vascular stenosis and atherosclerosis. However, it is not clear whether mast cells also regulate vascular matrix remodelling in established neointima. This study addressed the hypothesis that perivascular mast cells regulate neointimal matrix remodelling using a mouse vein graft model. Methods: The impact of mast cells on neointimal remodelling was investigated using mast cell-deficient animals in both normolipidaemic (Kit W-sh/W-sh ) and hyperlipidaemic (apoEconditions. The effect of perivascular mast cells on vascular matrix remodelling, including collagen and elastin deposition, was investigated using a local mast cell reconstitution method that selectively repopulated mast cells around the carotid artery (where the vein graft was inserted) in Kit W-sh/W-sh mice. Results: In normolipidaemic vein grafts (Kit W-sh/W-sh vs. the wild type control C57BL/6J), collagen synthesis was not affected by mast cell deficiency at 4 weeks. In contrast, neointimal elastin was reduced by 6.5-fold in mast cell-deficient Kit W-sh/W-sh mice, which was prevented by perivascular mast cell reconstitution. Mast cell deficiency induced a similar reduction in neointimal elastin in hyperlipidaemic mice (apoE -/-Kit W-sh/W-sh vs. apoE -/-), with a significant increase in cell proliferation and neointimal area at 4 weeks. Conclusion: Mast cells appear to promote elastin deposition in vein grafts and this may lead to further suppression of cell proliferation and neointimal thickening under hyperlipidaemic conditions. Key words:Mast cells, elastin, chronic restenosis, neointima, vein graft ABSTRACTArticle history:

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Mast Cells Contribute to Scar Formation during Fetal Wound Healing

Cited by 157 publications

References 52 publications

Mast Cells Are Dispensable for Normal and Activin-Promoted Wound Healing and Skin Carcinogenesis

Mast Cells Are Dispensable for Normal and Activin-Promoted Wound Healing and Skin Carcinogenesis

Pro‐Regenerative Hydrogel Restores Scarless Skin during Cutaneous Wound Healing

Perivascular mast cells promote neointimal elastin deposition and suppress chronic vein graft restenosis in hyperlipidaemic mice

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