Document Detail


Elastin signaling in wound repair.
MedLine Citation:
PMID:  23109320     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
Skin is an important organ to the human body as it functions as an interface between the body and environment. Cutaneous injury elicits a complex wound healing process, which is an orchestration of cells, matrix components, and signaling factors that re-establishes the barrier function of skin. In adults, an unavoidable consequence of wound healing is scar formation. However, in early fetal development, wound healing is scarless. This phenomenon is characterized by an attenuated inflammatory response, differential expression of signaling factors, and regeneration of normal skin architecture. Elastin endows a range of mechanical and cell interactive properties to skin. In adult wound healing, elastin is severely lacking and only a disorganized elastic fiber network is present after scar formation. The inherent properties of elastin make it a desirable inclusion to adult wound healing. Elastin imparts recoil and resistance and induces a range of cell activities, including cell migration and proliferation, matrix synthesis, and protease production. The effects of elastin align with the hallmarks of fetal scarless wound healing. Elastin synthesis is substantial in late stage in utero and drops to a trickle in adults. The physical and cell signaling advantages of elastin in a wound healing context creates a parallel with the innate features of fetal skin that can allow for scarless healing. Birth Defects Research (Part C) 96:248-257, 2012. © 2012 Wiley Periodicals, Inc.
Authors:
Jessica F Almine; Steven G Wise; Anthony S Weiss
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Birth defects research. Part C, Embryo today : reviews     Volume:  96     ISSN:  1542-9768     ISO Abbreviation:  Birth Defects Res. C Embryo Today     Publication Date:  2012 Sep 
Date Detail:
Created Date:  2012-10-30     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101167665     Medline TA:  Birth Defects Res C Embryo Today     Country:  United States    
Other Details:
Languages:  eng     Pagination:  248-57     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Wiley Periodicals, Inc.
Affiliation:
School of Molecular Bioscience, University of Sydney, New South Wales, Australia.
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