1
40
5
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
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
A name given to the resource
Glycoprotein Nonmelanoma Clone B Regulates the Crosstalk between Macrophages and Mesenchymal Stem Cells toward Wound Repair.
Publisher
An entity responsible for making the resource available
The Journal of investigative dermatology
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-01
Subject
The topic of the resource
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
An entity primarily responsible for making the resource
Yu Bing; Alboslemy Talib; Safadi Fayez; Kim Min-Ho
Description
An account of the resource
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
An unambiguous reference to the resource within a given context
<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
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1074/jbc.M114.624270" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/jbc.M114.624270</a>
Pages
20128–20146
Issue
33
Volume
290
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
A name given to the resource
Mutation in Osteoactivin Promotes Receptor Activator of NFkappaB Ligand (RANKL)-mediated Osteoclast Differentiation and Survival but Inhibits Osteoclast Function.
Publisher
An entity responsible for making the resource available
The Journal of biological chemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-08
Subject
The topic of the resource
*Mutation; Akt; Animals; bone; bone marrow; Bone Remodeling; Cell Differentiation/*physiology; Cell Survival/*physiology; Eye Proteins/*genetics; Inbred DBA; MAP kinases (MAPKs); Membrane Glycoproteins/*genetics; Mice; osteoactivin; osteoclast; Osteoclasts/*cytology; osteopetrosis; RANK Ligand/metabolism/*physiology; Signal Transduction; X-Ray Microtomography
Creator
An entity primarily responsible for making the resource
Abdelmagid Samir M; Sondag Gregory R; Moussa Fouad M; Belcher Joyce Y; Yu Bing; Stinnett Hilary; Novak Kimberly; Mbimba Thomas; Khol Matthew; Hankenson Kurt D; Malcuit Christopher; Safadi Fayez F
Description
An account of the resource
We previously reported on the importance of osteoactivin (OA/Gpnmb) in osteogenesis. In this study, we examined the role of OA in osteoclastogenesis, using mice with a nonsense mutation in the Gpnmb gene (D2J) and wild-type controls (D2J/Gpnmb(+)). In these D2J mice, micro-computed tomography and histomorphometric analyses revealed increased cortical thickness, whereas total porosity and eroded surface were significantly reduced in D2J mice compared with wild-type controls, and these results were corroborated by lower serum levels of
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1074/jbc.M114.624270" target="_blank" rel="noreferrer noopener">10.1074/jbc.M114.624270</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Mutation
2015
Abdelmagid Samir M
Akt
Animals
Belcher Joyce Y
Bone
bone marrow
Bone Remodeling
Cell Differentiation/*physiology
Cell Survival/*physiology
Department of Anatomy & Neurobiology
Eye Proteins/*genetics
Hankenson Kurt D
Inbred DBA
Khol Matthew
Malcuit Christopher
MAP kinases (MAPKs)
Mbimba Thomas
Membrane Glycoproteins/*genetics
Mice
Moussa Fouad M
NEOMED College of Medicine
Novak Kimberly
OSTEOACTIVIN
osteoclast
Osteoclasts/*cytology
osteopetrosis
RANK Ligand/metabolism/*physiology
Safadi Fayez F
Signal Transduction
Sondag Gregory R
Stinnett Hilary
The Journal of biological chemistry
X-Ray Microtomography
Yu Bing
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1038/emm.2016.78" target="_blank" rel="noreferrer noopener">http://doi.org/10.1038/emm.2016.78</a>
Pages
e257–e257
Issue
9
Volume
48
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
A name given to the resource
Osteoactivin inhibition of osteoclastogenesis is mediated through CD44-ERK signaling.
Publisher
An entity responsible for making the resource available
Experimental & molecular medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-09
Subject
The topic of the resource
*MAP Kinase Signaling System; *Signal Transduction; Animals; Cell Differentiation; Cells; Cultured; Eye Proteins/*metabolism; Hyaluronan Receptors/*metabolism; Inbred C57BL; Male; Membrane Glycoproteins/*metabolism; Mice; Osteoclasts/*cytology/metabolism; RANK Ligand/metabolism; Recombinant Proteins/metabolism
Creator
An entity primarily responsible for making the resource
Sondag Gregory R; Mbimba Thomas S; Moussa Fouad M; Novak Kimberly; Yu Bing; Jaber Fatima A; Abdelmagid Samir M; Geldenhuys Werner J; Safadi Fayez F
Description
An account of the resource
Osteoactivin is a heavily glycosylated protein shown to have a role in bone remodeling. Previous studies from our lab have shown that mutation in Osteoactivin enhances osteoclast differentiation but inhibits their function. To date, a classical receptor and a signaling pathway for Osteoactivin-mediated osteoclast inhibition has not yet been characterized. In this study, we examined the role of Osteoactivin treatment on osteoclastogenesis using bone marrow-derived osteoclast progenitor cells and identify a signaling pathway relating to Osteoactivin function. We reveal that recombinant Osteoactivin treatment inhibited osteoclast differentiation in a dose-dependent manner shown by qPCR, TRAP staining, activity and count. Using several approaches, we show that Osteoactivin binds CD44 in osteoclasts. Furthermore, recombinant Osteoactivin treatment inhibited ERK phosphorylation in a CD44-dependent manner. Finally, we examined the role of Osteoactivin on receptor activator of nuclear factor-kappa B ligand (RANKL)-induced osteolysis in vivo. Our data indicate that recombinant Osteoactivin inhibits RANKL-induced osteolysis in vivo and this effect is CD44-dependent. Overall, our data indicate that Osteoactivin is a negative regulator of osteoclastogenesis in vitro and in vivo and that this process is regulated through CD44 and ERK activation.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1038/emm.2016.78" target="_blank" rel="noreferrer noopener">10.1038/emm.2016.78</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*MAP Kinase Signaling System
*Signal Transduction
2016
Abdelmagid Samir M
Animals
Cell Differentiation
Cells
Cultured
Department of Anatomy & Neurobiology
Experimental & molecular medicine
Eye Proteins/*metabolism
Geldenhuys Werner J
Hyaluronan Receptors/*metabolism
Inbred C57BL
Jaber Fatima A
Male
Mbimba Thomas S
Membrane Glycoproteins/*metabolism
Mice
Moussa Fouad M
NEOMED College of Medicine
Novak Kimberly
Osteoclasts/*cytology/metabolism
RANK Ligand/metabolism
Recombinant Proteins/metabolism
Safadi Fayez F
Sondag Gregory R
Yu Bing
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
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>
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
A name given to the resource
Glycoprotein Nonmelanoma Clone B Regulates the Crosstalk between Macrophages and Mesenchymal Stem Cells toward Wound Repair.
Publisher
An entity responsible for making the resource available
The Journal of investigative dermatology
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-01
Creator
An entity primarily responsible for making the resource
Yu Bing; Alboslemy Talib; Safadi Fayez; Kim Min-Ho
Description
An account of the resource
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
An unambiguous reference to the resource within a given context
<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>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2018
Alboslemy Talib
Department of Anatomy & Neurobiology
Kim Min-Ho
NEOMED College of Medicine
Safadi Fayez
The Journal of investigative dermatology
Yu Bing
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1002/jcb.25394" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/jcb.25394</a>
Pages
1511–1521
Issue
7
Volume
117
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
A name given to the resource
Macrophage-Associated Osteoactivin/GPNMB Mediates Mesenchymal Stem Cell Survival, Proliferation, and Migration Via a CD44-Dependent Mechanism.
Publisher
An entity responsible for making the resource available
Journal of cellular biochemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-07
Subject
The topic of the resource
*CD44; *M2 MACROPHAGES; *MSC; *OA/GPNMB; Animals; Cell Movement/*physiology; Cell Proliferation/*physiology; Cell Survival/physiology; Eye Proteins/genetics/*metabolism; Hyaluronan Receptors/genetics/*metabolism; Knockout; Macrophages/cytology/*metabolism; MAP Kinase Signaling System/physiology; Membrane Glycoproteins/genetics/*metabolism; Mesenchymal Stem Cells/cytology/*metabolism; Mice
Creator
An entity primarily responsible for making the resource
Yu Bing; Sondag Gregory R; Malcuit Christopher; Kim Min-Ho; Safadi Fayez F
Description
An account of the resource
Although MSCs have been widely recognized to have therapeutic potential in the repair of injured or diseased tissues, it remains unclear how functional activities of mesenchymal stem cells (MSCs) are influenced by the surrounding inflammatory milieu at the site of tissue injury. Macrophages constitute an essential component of innate immunity and have been shown to exhibit a phenotypic plasticity in response to various stimuli, which play a central role in both acute inflammation and wound repair. Osteoactivin (OA)/Glycoprotein non-metastatic melanoma protein B (GPNMB), a transmembrane glycoprotein that plays a role in cell differentiation, survival, and angiogenesis. The objective of this study was to investigate the potential role of OA/GPNMB in macrophage-induced MSC function. We found that reparative M2 macrophages express significantly greater levels of OA/GPNMB than pro-inflammatory M1 macrophages. Furthermore, using loss of function and rescue studies, we demonstrated that M2 macrophages-secreted OA/GPNMB positively regulates the viability, proliferation, and migration of MSCs. More importantly, we demonstrated that OA/GPNMB acts through ERK and AKT signaling pathways in MSCs via CD44, to induce these effects. Taken together, our results provide pivotal insight into the mechanism by which OA/GPNMB contributes to the tissue reparative phenotype of M2 macrophages and positively regulates functional activities of MSCs. J. Cell. Biochem. 117:
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/jcb.25394" target="_blank" rel="noreferrer noopener">10.1002/jcb.25394</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*CD44
*M2 MACROPHAGES
*MSC
*OA/GPNMB
2016
Animals
Cell Movement/*physiology
Cell Proliferation/*physiology
Cell Survival/physiology
Department of Anatomy & Neurobiology
Eye Proteins/genetics/*metabolism
Hyaluronan Receptors/genetics/*metabolism
Journal of cellular biochemistry
Kim Min-Ho
Knockout
Macrophages/cytology/*metabolism
Malcuit Christopher
MAP Kinase Signaling System/physiology
Membrane Glycoproteins/genetics/*metabolism
Mesenchymal Stem Cells/cytology/*metabolism
Mice
NEOMED College of Medicine
Safadi Fayez F
Sondag Gregory R
Yu Bing