Skin Wound Healing and Scarring: Fetal Wounds and Regenerative Restitution

Yates, Cecelia C.; Hebda, Patricia A.; Wells, Alan

doi:10.1002/bdrc.21024

Cited by 131 publications

(94 citation statements)

References 92 publications

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“…In future studies it will be informative to perform live imaging of fiber architecture over time to determine whether Mmp9 regulates the transition in fiber thickness as wound healing progresses. It is known that, following injury in mammalian models, surrounding fibroblasts rapidly produce collagen (Eickelberg et al, 1999;Yates et al, 2012), providing a transient matrix for stability. The type of collagen produced appears to be age dependent and coincides with whether a wound scars or regenerates.…”

Section: Discussionmentioning

confidence: 99%

“…The type of collagen produced appears to be age dependent and coincides with whether a wound scars or regenerates. Adult wound-induced ECM is predominately the thicker type I collagen, whereas fetal woundinduced collagen is the thinner type III collagen (Yates et al, 2012). SHG imaging does not discriminate between type I and III collagen, and it is therefore possible that Mmp9 is involved in a switch in collagen type during repair.…”

Section: Discussionmentioning

confidence: 99%

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Matrix metalloproteinase 9 modulates collagen matrices and wound repair

et al. 2015

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Acute and chronic injuries are characterized by leukocyte infiltration into tissues. Although matrix metalloproteinase 9 (Mmp9) has been implicated in both conditions, its role in wound repair remains unclear. We previously reported a zebrafish chronic inflammation mutant caused by an insertion in the hepatocyte growth factor activator inhibitor gene 1 (hai1; also known as spint1) that is characterized by epithelial extrusions and neutrophil infiltration into the fin. Here, we performed a microarray analysis and found increased inflammatory gene expression in the mutant larvae, including a marked increase in mmp9 expression. Depletion of mmp9 partially rescued the chronic inflammation and epithelial phenotypes, in addition to restoring collagen fiber organization, as detected by second-harmonic generation imaging. Additionally, we found that acute wounding induces epithelial cell mmp9 expression and is associated with a thickening of collagen fibers. Interestingly, depletion of mmp9 impaired this collagen fiber reorganization. Moreover, mmp9 depletion impaired tissue regeneration after tail transection, implicating Mmp9 in acute wound repair. Thus, Mmp9 regulates both acute and chronic tissue damage and plays an essential role in collagen reorganization during wound repair.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Matrix metalloproteinase 9 modulates collagen matrices and wound repair

et al. 2015

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“…Despite the fact that deposition of extracellular matrix in the fetal wound healing process is similar to the adult one, the temporal and spatial distribution of fetal extracellular matrix is different from its adult counterpart. Compared to adults, the production and precipitation of extracellular matrix by fetal fibroblasts is much more coordinated with stronger synthetic and secretory phenotype (5,6). Fetal skin repair beCopyright © 2018, Archives of Neuroscience.…”

Section: Introductionmentioning

confidence: 99%

GMP-Compliant Human Fetal Skin Fibroblasts for Wound Healing

et al. 2018

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Background: Among different kinds of cells involved in the wound healing process, fibroblasts play a pivotal role in the proliferation phase of this procedure wherein they induce the production of local growth factors and cytokines. Fetal fibroblasts with low immunogenic property and different wound healing process could be considered as a suitable alternative to neonatal foreskin cell based products in regenerative medicine and cell therapy. Cell therapy is an almost newly introduced method in the medical field and is also a challenging issue, which should assure the safety of the final product and the absence of viral or bacterial contamination with minimal immunogenic response. Therefore, based on current GMP (cGMP) principles, it is a matter of great importance to monitor raw materials' quality and the conformity of all production procedures including cell culture, collection, and cryopreservation with validated standard operating procedures (SOPs). In the current study, we demonstrated the GMP-compatible and clinical-grade fetal fibroblast cells banking to be used for clinical applications. Methods: All steps of isolation and culturing and cryopreservation of fetal fibroblast cells were performed under the sterile condition according to cGMP guidelines in the clean room. During the cell culture procedures, bacteriological investigation was performed in order to identify the probable contamination of the samples.

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“…It should progress in a coordinated manner and requires the presence of various biological mediators and growth factors [1][2][3][4][5][6][7]. Disruption of this coordination results in abnormal healing; persistence inflammatory phase causes chronic wound [8] and persistence of remodelling phase causes excessive scarring [9]. Moreover, sustained release of cytokines results in continued cell proliferation and tissue remodelling [10] leading to keloid formation, one of the major abnormity of wound healing [11,12].…”

Section: Introductionmentioning

confidence: 99%

Co-upregulation of Transforming Growth Factor Beta-1 and Nitric Oxide Synthase in Keloid by comparison to normal human skin-A possible role for TGFβ1 and NOS in pathogenesis of keloid

El-Aleem¹,

Abdelwahab²,

Osman³

2017

J Cytol Histol

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Keloid disease is a benign but progressive form of abnormal wound healing associated with skin fibrosis and can cause a major functional disability and morbidity. TGF beta (TGFβ) and Nitric Oxide (NO) are active biomarkers known to regulate phases of wound healing and have been implicated in pathogenesis of fibrotic disease. There are three isoforms of TGFβ (1, 2 and 3) TGFβ1 and 3 have a crucial role in fibrosis, with TGFβ1 profibrotic and TGFβ3 antifibrotic. NO is produced by Nitric Oxide Synthase (NOS) which exist in three isoforms, inducible NOS (iNOS), endothelial NOS (ecNOS) and neuronal NOS (nNOS). TGFβ isoforms and NO were found to be associated with fibrotic disorders affecting the skin. We hypothesis that the interaction between TGFβ and NO in keloid could promote the excessive collagen deposition associated with this disorder.Using immunohistochemistry, we investigated the profile of TGFβ isoforms (TGFβ1, 3) and NOS isoforms (iNOS and ecNOS) in keloid tissues and normal human skin. The cellular distribution of all the isoforms were studied and the protein levels were assessed by using H-Scoring and Image J Scoring systems.

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Skin Wound Healing and Scarring: Fetal Wounds and Regenerative Restitution

Cited by 131 publications

References 92 publications

Matrix metalloproteinase 9 modulates collagen matrices and wound repair

Matrix metalloproteinase 9 modulates collagen matrices and wound repair

GMP-Compliant Human Fetal Skin Fibroblasts for Wound Healing

Co-upregulation of Transforming Growth Factor Beta-1 and Nitric Oxide Synthase in Keloid by comparison to normal human skin-A possible role for TGFβ1 and NOS in pathogenesis of keloid

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