Fibromodulin Is Essential for Fetal-Type Scarless Cutaneous Wound Healing

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Penn collection
Departmental Papers (Dental)
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Animals
Cicatrix
Collagen
Female
Fetus
Fibromodulin
Gene Expression Profiling
Gene Expression Regulation
Gestational Age
Male
Mice
Oligonucleotide Array Sequence Analysis
Rats
Rats
Sprague-Dawley
Skin
Transforming Growth Factor beta1
Wound Healing
collagen
collagen type 1
fibromodulin
leucine
proteoglycan
transforming growth factor beta1
collagen
fibromodulin
transforming growth factor beta1
angiogenesis
animal experiment
animal model
animal tissue
Article
clinical evaluation
controlled study
disease association
embryo development
female
fetus
gain of function mutation
gestational age
male
nonhuman
priority journal
protein expression
rat
scarless cutaneous wound healing
skin injury
wound healing
animal
DNA microarray
embryology
gene expression profiling
gene expression regulation
genetics
injuries
metabolism
mouse
pathology
scar
skin
Sprague Dawley rat
Dental Materials
Dentistry
Oral and Maxillofacial Surgery
Orthodontics and Orthodontology
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Author
Zheng, Zhong
Zhang, Xinli
Dang, Catherine
Beanes, Steven
Chang, Grace X.
Chen, Yao
Li, Chen-Shuang
Lee, Kevin S.
Ting, Kang
Soo, Chia
Contributor
Abstract

In contrast to adult and late-gestation fetal skin wounds, which heal with scar, early-gestation fetal skin wounds display a remarkable capacity to heal scarlessly. Although the underlying mechanism of this transition from fetal-type scarless healing to adult-type healing with scar has been actively investigated for decades, in utero restoration of scarless healing in late-gestation fetal wounds has not been reported. In this study, using loss- and gain-of-function rodent fetal wound models, we identified that fibromodulin (Fm) is essential for fetal-type scarless wound healing. In particular, we found that loss of Fm can eliminate the ability of early-gestation fetal rodents to heal without scar. Meanwhile, administration of fibromodulin protein (FM) alone was capable of restoring scarless healing in late-gestation rat fetal wounds, which naturally heal with scar, as characterized by dermal appendage restoration and organized collagen architectures that were virtually indistinguishable from those in age-matched unwounded skin. High Fm levels correlated with decreased transforming growth factor (TGF)-β1 expression and scarless repair, while low Fm levels correlated with increased TGF-β1 expression and scar formation. This study represents the first successful in utero attempt to induce scarless repair in late-gestation fetal wounds by using a single protein, Fm, and highlights the crucial role that the FM–TGF-β1 nexus plays in fetal-type scarless skin repair. © 2016 American Society for Investigative Pathology

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2016-11-01
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American Journal of Pathology
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At the time of publication, author Chenshuang Li was affiliated with the School of Dentistry, University of California. Currently, (s)he is a faculty member at the School of Dental Medicine at the University of Pennsylvania.
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