Cell surface engineering using glycosylphosphatidylinositol anchored tissue inhibitor of matrix metalloproteinase‐1 stimulates cutaneous wound healing

Djafarzadeh, Roghieh; Conrad, Claudius; Notohamiprodjo, Susan; Hipp, Stephanie; Nieß, Hanno; Bruns, Christiane; Nelson, Peter J.

doi:10.1111/wrr.12132

Cited by 8 publications

(9 citation statements)

References 29 publications

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“…In other studies, incorporation of TIMP-1 into the surface of human dermal fibroblasts using a glycosylphosphatidylinositol anchor resulted in reduced secretion of MMP-2 and MMP-9, reduced migration and proliferation of fibroblasts, and reduced expression of profibrotic genes. 29 , 52 These results, which are logically similar to those caused by MMP-inhibitor GM6001, suggest that TIMPs could be therapeutic, perhaps in the margins of keloids. The peripheral collagen being degraded by MMPs offers another therapeutic target.…”

Section: Therapeutic Approaches Involving Mmpsmentioning

confidence: 81%

High-mobility Group Box Protein-1, Matrix Metalloproteinases, and Vitamin D in Keloids and Hypertrophic Scars

Lee

Trowbridge

Ayoub

et al. 2015

Plastic and Reconstructive Surgery - Global Open

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Summary:Keloids and hypertrophic scars represent excessive wound healing involving high production of collagen by skin fibroblasts. This review focuses on the role of high-mobility group box protein-1 (HMGB-1), matrix metalloproteinases (MMPs), and vitamin D in these conditions. Although the role of HMGB-1 in keloids and hypertrophic scars is unclear, the effect of HMGB-1 on fibroblasts suggests a profibrotic role and a potential contribution to excessive scarring. MMPs contribute extensively to wound healing and characteristically degrade the extracellular matrix. MMP-1 is decreased in keloids and hypertrophic scars. However, other MMPs, including MMP-2, have been found to be increased and are thought to possibly contribute to keloid expansion through peripheral extracellular matrix catabolism. Many novel therapeutic approaches to keloids and hypertrophic scars target MMPs and aim to increase their levels and catabolic activity. The higher prevalence of keloids in darker skin types may partially be due to a tendency for lower vitamin D levels. The physiologically active form of vitamin D, 1,25(OH)2D3, inhibits the proliferation of keloid fibroblasts, and correlations between vitamin D receptor polymorphisms, such as the TaqI CC genotype, and keloid formation have been reported. Additionally, vitamin D may exert an antifibrotic effect partially mediated by MMPs. Here, we critically discuss whether keloid and hypertrophic scar formation could be predicted based on vitamin D status and vitamin D receptor polymorphisms. Specifically, the findings identified HMGB-1, MMPs, and vitamin D as potential avenues for further clinical investigation and potentially novel therapeutic approaches to prevent the development of keloids and hypertrophic scars.

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Section: Therapeutic Approaches Involving Mmpsmentioning

confidence: 81%

High-mobility Group Box Protein-1, Matrix Metalloproteinases, and Vitamin D in Keloids and Hypertrophic Scars

Lee

Trowbridge

Ayoub

et al. 2015

Plastic and Reconstructive Surgery - Global Open

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“…In addition, TIMP1 has been shown to promote growth and inhibit apoptosis of cells related to wound healing (Djafarzadeh et al . ).…”

Section: Introductionmentioning

confidence: 97%

Effect of tissue inhibitor of metalloprotease 1 on human pulp cells in vitro and rat pulp tissue in vivo

et al. 2019

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Aim To evaluate the dentinogenetic effects of tissue inhibitor of metalloprotease (TIMP1) on human pulp cells in vitro and rat pulp tissue in vivo. Methodology The effect of TIMP1 on pulp cell functions related to hard tissue formation as part of the wound healing process (i.e. biocompatibility, proliferation, differentiation and mineralized nodule formation) was evaluated in vitro and using a direct pulp capping experimental animal model in vivo. The effects of different‐sized cavity preparations on hard tissue formation induced by ProRoot MTA at 2 weeks were evaluated using micro‐computed tomography (micro‐CT). Tertiary dentine formation quality and quantity after pulp capping using TIMP1, ProRoot MTA and phosphate‐buffered saline (PBS) was also evaluated after 4 weeks using micro‐CT in term of dentine volume (DV), dentine mineral density (DVD) and histological analysis. The data were evaluated by Student's t‐test, one‐way ANOVA with Tukey's post hoc test, the Kruskal–Wallis test or the Steel–Dwass test. P values < 0.05 were considered statistically significant. Results TIMP1 significantly stimulated dental pulp stem cell proliferation, differentiation, and mineralization and was more biocompatible compared with the PBS control (P < 0.05). In the pulp capping model, the amount of tertiary dentine that formed was directly proportional to the size of the pulp exposure; greater amounts of tertiary dentine were observed in pulps with larger exposures after 2 weeks. 4‐week samples of TIMP1 and ProRoot MTA had similar characteristics, but both sample significantly induced tertiary dentine formation beneath the cavity compared with PBS (P < 0.05) under standardized cavity preparations. Conclusions TIMP1 has an important role in pulpal wound healing, which makes it a potential biological pulp capping material and candidate molecule for regenerative endodontic therapy.

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“…While both the mode of action (decreased flexibility of the extracellular matrix) and delivery (direct GPI-AP delivery to the tumors and on-site integration) seem feasible and in vivo mouse models yield promising data, further preclinical and clinical research is needed. Other medical conditions that may be targeted by GPI-AP membrane engineering include wound healing, again by using TIMP-1 ( 74 , 75 ), or manipulation of the protein C system involved in anti-coagulant and cyto-protective processes ( 76 ). Also, gram-negative bacteria have been modified by MP.…”

Section: Modification Of Cellsmentioning

confidence: 99%

Biomedical applications of glycosylphosphatidylinositol-anchored proteins

Heider

Dangerfield²,

Metzner

2016

Journal of Lipid Research

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Glycosylphosphatidylinositol (GPI)-anchored proteins (GPI-APs) use a unique posttranslational modification to link proteins to lipid bilayer membranes. The anchoring structure consists of both a lipid and carbohydrate portion and is highly conserved in eukaryotic organisms regarding its basic characteristics, yet highly variable in its molecular details. The strong membrane targeting property has made the anchors an interesting tool for biotechnological modification of lipid membrane-covered entities from cells through extracellular vesicles to enveloped virus particles. In this review, we will take a closer look at the mechanisms and fields of application for GPI-APs in lipid bilayer membrane engineering and discuss their advantages and disadvantages for biomedicine.

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Cell surface engineering using glycosylphosphatidylinositol anchored tissue inhibitor of matrix metalloproteinase‐1 stimulates cutaneous wound healing

Cited by 8 publications

References 29 publications

High-mobility Group Box Protein-1, Matrix Metalloproteinases, and Vitamin D in Keloids and Hypertrophic Scars

High-mobility Group Box Protein-1, Matrix Metalloproteinases, and Vitamin D in Keloids and Hypertrophic Scars

Effect of tissue inhibitor of metalloprotease 1 on human pulp cells in vitro and rat pulp tissue in vivo

Biomedical applications of glycosylphosphatidylinositol-anchored proteins

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