Type I and Type III Collagen Content of Healing Wounds in Fetal and Adult Rats

Merkel, Joseph R.; DiPaolo, Byron R.; Hallock, Geoffrey G.; Rice, David C.

doi:10.3181/00379727-187-42694

Cited by 190 publications

(121 citation statements)

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“…It has been shown that collagen subtype deposition may predict future scar formation. In fact, the fetal skin, the best model for scarless healing, is known to contain a greater proportion of type III collagen in comparison with type I collagen and this differential collagen deposition during fetal skin healing is thought to contribute to scarless wound healing (48). In this study, we observed that GF wounds have a higher proportion of type III collagen as well as a minimum area of scar tissue.…”

Section: Discussionsupporting

confidence: 66%

Skin Wound Healing Is Accelerated and Scarless in the Absence of Commensal Microbiota

Canesso

Vieira

Castro

et al. 2014

The Journal of Immunology

149

126

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The commensal microbiota has a high impact on health and disease by modulating the development and homeostasis of host immune system. Immune cells are involved in virtually every aspect of the wound repair process; however, the impact of commensal microbiota on skin wound healing is largely unknown. In this study, we evaluated the influence of commensal microbiota on tissue repair of excisional skin wounds by using germ-free (GF) Swiss mice. We observed that macroscopic wound closure rate is accelerated in the absence of commensal microbiota. Accordantly, histologically assessed wound epithelization was accelerated in GF in comparison with conventional (CV) Swiss mice. The wounds of GF mice presented a significant decrease in neutrophil accumulation and an increase in mast cell and macrophage infiltration into wounds. Interestingly, alternatively activated healing macrophage-related genes were highly expressed in the wound tissue of GF mice. Moreover, levels of the anti-inflammatory cytokine IL-10, the angiogenic growth factor VEGF and angiogenesis were higher in the wound tissue of those mice. Conversely, scarring and levels of the profibrogenic factor TGF-β1 were greatly reduced in GF mice wounded skin when compared with CV mice. Of note, conventionalization of GF mice with CV microbiota restored wound closure rate, neutrophil and macrophage accumulation, cytokine production, and scarring to the same extent as CV mice. Overall, our findings suggest that, in the absence of any contact with microbiota, skin wound healing is accelerated and scarless, partially because of reduced accumulation of neutrophils, increased accumulation of alternatively activated healing macrophages, and better angiogenesis at wound sites.

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Section: Discussionsupporting

confidence: 66%

Skin Wound Healing Is Accelerated and Scarless in the Absence of Commensal Microbiota

Canesso

Vieira

Castro

et al. 2014

The Journal of Immunology

149

126

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“…Turnover rates of fibrillar collagens are generally low, with the periodontal ligament representing an exception (Sodek and Ferrier, 1988), but the cell-collagen interactions show a dynamic relationship during tissue regeneration events, such as wound healing, when fibroblasts of various origins are recruited and produce a wound matrix that is rich in fibrillar collagens (Schäfer and Werner, 2008). These include collagen type III with a smaller fibril diameter that, as the granulation tissue matures, is replaced with collagen I (Merkel et al, 1988). In fibrosis, overproduction of fibrillar collagen causes tissue dysfunction, but the role of the fibrillar collagen-rich tumor stroma is still a matter for debate.…”

Section: Collagen-binding Integrins In the Tumor Stromamentioning

confidence: 99%

The integrin–collagen connection – a glue for tissue repair?

Zeltz

Gullberg

2016

Journal of Cell Science

174

126

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There was an error published in J. Cell Sci. 129, 653-664.In Fig. 2A, the fibroblasts were incorrectly labelled. The correct annotation should have been α11 −/− fibroblast (left) and α11 +/+ fibroblast (right). The correct Fig. 2 is shown below. We apologise to the readers for any confusion that this error might have caused. Journal of Cell Science COMMENTARYThe integrin-collagen connection -a glue for tissue repair?Cedric Zeltz and Donald Gullberg* ABSTRACTThe α1β1, α2β1, α10β1 and α11β1 integrins constitute a subset of the integrin family with affinity for GFOGER-like sequences in collagens.Integrins α1β1 and α2β1 were originally identified on a subset of activated T-cells, and have since been found to be expressed on a number of cell types including platelets (α2β1), vascular cells (α1β1, α2β1), epithelial cells (α1β1, α2β1) and fibroblasts (α1β1, α2β1).Integrin α10β1 shows a distribution that is restricted to mesenchymal stem cells and chondrocytes, whereas integrin α11β1 appears restricted to mesenchymal stem cells and subsets of fibroblasts. The bulk of the current literature suggests that collagen-binding integrins only have a limited role in adult connective tissue homeostasis, partly due to a limited availability of cell-binding sites in the mature fibrillar collagen matrices. However, some recent data suggest that, instead, they are more crucial for dynamic connective tissue remodeling events -such as wound healing -where they might act specifically to remodel and restore the tissue architecture. This Commentary discusses the recent development in the field of collagen-binding integrins, their roles in physiological and pathological settings with special emphasis on wound healing, fibrosis and tumor-stroma interactions, and include a discussion of the most recently identified newcomers to this subfamilyintegrins α10β1 and α11β1.

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“…Although collagen I is the predominant component of ECM in both the fetus and the adult, the quantity of collagen in fetal skin is lower than that in adult skin and a ratio of collagen III to collagen I in skin is higher in the fetus than in the adult. 65,66 In scarless fetal skin, collagen III comprises *30-60% of the total collagen compared to 10-20% in adult skin. 66,67 Wounding in this unique setting triggers a complex cascade of tightly controlled events resulting in a scarless phenotype, typically consisting of fine reticular collagen and abundant HA.…”

Section: Ecm Remodelling In Fetal Cutaneous Scarless Healingmentioning

confidence: 99%

Extracellular Matrix Reorganization During Wound Healing and Its Impact on Abnormal Scarring

Xue

Jackson

2015

Advances in Wound Care

992

866

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Significance: When a cutaneous injury occurs, the wound heals via a dynamic series of physiological events, including coagulation, granulation tissue formation, re-epithelialization, and extracellular matrix (ECM) remodeling. The final stage can take many months, yet the new ECM forms a scar that never achieves the flexibility or strength of the original tissue. In certain circumstances, the normal scar is replaced by pathological fibrotic tissue, which results in hypertrophic or keloid scars. These scars cause significant morbidity through physical dysfunction and psychological stress. Recent Advances and Critical Issues: The cutaneous ECM comprises a complex assortment of proteins that was traditionally thought to simply provide structural integrity and scaffolding characteristics. However, recent findings show that the ECM has multiple functions, including, storage and delivery of growth factors and cytokines, tissue repair and various physiological functions. Abnormal ECM reconstruction during wound healing contributes to the formation of hypertrophic and keloid scars. Whereas adult wounds heal with scarring, the developing foetus has the ability to heal wounds in a scarless fashion by regenerating skin and restoring the normal ECM architecture, strength, and function. Recent studies show that the lack of inflammation in fetal wounds contributes to this perfect healing. Future Directions: Better understanding of the exact roles of ECM components in scarring will allow us to produce therapeutic agents to prevent hypertrophic and keloid scars. This review will focus on the components of the ECM and their role in both physiological and pathological (hypertrophic and keloid) cutaneous scar formation. SCOPE AND SIGNIFICANCEThis article reviews the extracellular matrix (ECM) and its remodeling during normal cutaneous wound healing and scar formation, and the differential response of the components of the ECM and their role in pathological (hypertrophic and keloid) cutaneous scar formation. This review focuses on the major players involved in the irregular ECM production as being; fibroblasts and their immature counterparts, myofibroblasts; collagens; transforming growth factor (TGF)-b, which controls the production of collagens; proteoglycans and matrix metalloproteinases (MMPs). We also highlight the complexity of interactions occurring in the ECM of skin during (ab) normal scar formation. TRANSLATIONAL RELEVANCEAbnormal ECM, particularly abnormal collagen remodeling and reorganization, accounts for one of the most important contributing factors to abnormal scarring. Identification of the exact ECM molecules involved in causing abnormal scarring is likely to provide a future treatment target. This may be achieved by promoting the correct balance in collagen ratios or by directly targeting the production of collagen. Overall, a better understanding of the exact roles of ECM components in scarring will help us to produce therapeutic agents to prevent and treat hypertrophic and keloid scars. CLINICAL RELEVANCEThere ...

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Type I and Type III Collagen Content of Healing Wounds in Fetal and Adult Rats

Cited by 190 publications

References 0 publications

Skin Wound Healing Is Accelerated and Scarless in the Absence of Commensal Microbiota

Skin Wound Healing Is Accelerated and Scarless in the Absence of Commensal Microbiota

The integrin–collagen connection – a glue for tissue repair?

Extracellular Matrix Reorganization During Wound Healing and Its Impact on Abnormal Scarring

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