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Text
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URL Address
<a href="http://doi.org/10.1016/j.jid.2017.08.034" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.jid.2017.08.034</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
219-227
Issue
1
Volume
138
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Glycoprotein Nonmelanoma Clone B Regulates the Crosstalk between Macrophages and Mesenchymal Stem Cells toward Wound Repair.
Publisher
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The Journal of investigative dermatology
Date
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2018
2018-01
Subject
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Humans; Male; Animals; Mice; Cell Differentiation; Wound Healing/*physiology; Macrophages/*physiology; Diabetes Mellitus; Cells; Cultured; Inbred C57BL; Animal; Disease Models; Administration; Cutaneous; Cell Communication/*physiology; Eye Proteins/administration & dosage/genetics/*physiology; Membrane Glycoproteins/administration & dosage/genetics/*physiology; Mesenchymal Stem Cells/*physiology; Recombinant Proteins/administration & dosage/genetics/metabolism; Skin/*injuries/metabolism; Type 2/complications/pathology
Creator
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Yu Bing; Alboslemy Talib; Safadi Fayez; Kim Min-Ho
Description
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The process of wound repair requires the coordinated participation of multiple types of cells, which are sequentially recruited during the healing process. In response to tissue injury, both macrophages and mesenchymal stem cells (MSCs) are recruited to the site of injury, where they participate in the repair process. Despite considerable understanding of the role of each cell type in the process of wound repair, the nature of the dynamic interplay between these two cell types and how this interaction influences the process of wound repair are not well understood. Here, using an in vivo model of cutaneous wound healing in mice, we provide evidence that GPNMB is functionally important in promoting the recruitment of MSCs to the site of skin injury, which in turn modulates inflammatory responses by directing the M2 polarization of macrophages in acute wound healing. Furthermore, we show that GPNMB activity is impaired in a diabetic wound environment, which is associated with impaired MSC recruitment that is reversed by the topical administration of recombinant GPNMB protein to the wounds of diabetic mice. Our study provides important insight into the crosstalk between macrophages and endogenous MSCs toward wound repair.
Identifier
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<a href="http://doi.org/10.1016/j.jid.2017.08.034" target="_blank" rel="noreferrer noopener">10.1016/j.jid.2017.08.034</a>
2018
Administration
Alboslemy Talib
Animal
Animals
Cell Communication/*physiology
Cell Differentiation
Cells
Cultured
Cutaneous
Diabetes Mellitus
Disease Models
Eye Proteins/administration & dosage/genetics/*physiology
Humans
Inbred C57BL
Kim Min-Ho
Macrophages/*physiology
Male
Membrane Glycoproteins/administration & dosage/genetics/*physiology
Mesenchymal Stem Cells/*physiology
Mice
Recombinant Proteins/administration & dosage/genetics/metabolism
Safadi Fayez
Skin/*injuries/metabolism
The Journal of investigative dermatology
Type 2/complications/pathology
Wound Healing/*physiology
Yu Bing