1
40
4
-
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/10.1128/JVI.03156-15" target="_blank" rel="noreferrer noopener">http://doi.org/10.1128/JVI.03156-15</a>
Pages
3385–3399
Issue
7
Volume
90
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
Ecotropic Murine Leukemia Virus Infection of Glial Progenitors Interferes with Oligodendrocyte Differentiation: Implications for Neurovirulence.
Publisher
An entity responsible for making the resource available
Journal of virology
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-01
Subject
The topic of the resource
3T3 Cells; Animals; Cell Line; Cell Proliferation; Cell Survival; env/biosynthesis; Female; Gene Products; Leukemia Virus; Male; Mice; Motor Neuron Disease/*virology; Murine/*pathogenicity; Neural Stem Cells/*virology; Neurogenesis/*physiology; Neuroglia/*virology; Oligodendroglia/cytology/virology; Retroviridae Infections/*complications; Transgenic
Creator
An entity primarily responsible for making the resource
Li Ying; Dunphy Jaclyn M; Pedraza Carlos E; Lynch Connor R; Cardona Sandra M; Macklin Wendy B; Lynch William P
Description
An account of the resource
UNLABELLED: Certain murine leukemia viruses (MLVs) are capable of inducing fatal progressive spongiform motor neuron disease in mice that is largely mediated by viral Env glycoprotein expression within central nervous system (CNS) glia. While the etiologic mechanisms and the glial subtypes involved remain unresolved, infection of NG2 glia was recently observed to correlate spatially and temporally with altered neuronal physiology and spongiogenesis. Since one role of NG2 cells is to serve as oligodendrocyte (OL) progenitor cells (OPCs), we examined here whether their infection by neurovirulent (FrCasE) or nonneurovirulent (Fr57E) ecotropic MLVs influenced their viability and/or differentiation. Here, we demonstrate that OPCs, but not OLs, are major CNS targets of both FrCasE and Fr57E. We also show that MLV infection of neural progenitor cells (NPCs) in culture did not affect survival, proliferation, or OPC progenitor marker expression but suppressed certain glial differentiation markers. Assessment of glial differentiation in vivo using transplanted transgenic NPCs showed that, while MLVs did not affect cellular engraftment or survival, they did inhibit OL differentiation, irrespective of MLV neurovirulence. In addition, in chimeric brains, where FrCasE-infected NPC transplants caused neurodegeneration, the transplanted NPCs proliferated. These results suggest that MLV infection is not directly cytotoxic to OPCs but rather acts to interfere with OL differentiation. Since both FrCasE and Fr57E viruses restrict OL differentiation but only FrCasE induces overt neurodegeneration, restriction of OL maturation alone cannot account for neuropathogenesis. Instead neurodegeneration may involve a two-hit scenario where interference with OPC differentiation combined with glial Env-induced neuronal hyperexcitability precipitates disease. IMPORTANCE: A variety of human and animal retroviruses are capable of causing central nervous system (CNS) neurodegeneration manifested as motor and cognitive deficits. These retroviruses infect a variety of CNS cell types; however, the specific role each cell type plays in neuropathogenesis remains to be established. The NG2 glia, whose CNS functions are only now emerging, are a newly appreciated viral target in murine leukemia virus (MLV)-induced neurodegeneration. Since one role of NG2 glia is that of oligodendrocyte progenitor cells (OPCs), we investigated here whether their infection by the neurovirulent MLV FrCasE contributed to neurodegeneration by affecting OPC viability and/or development. Our results show that both neurovirulent and nonneurovirulent MLVs interfere with oligodendrocyte differentiation. Thus, NG2 glial infection could contribute to neurodegeneration by preventing myelin formation and/or repair and by suspending OPCs in a state of persistent susceptibility to excitotoxic insult mediated by neurovirulent virus effects on other glial subtypes.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1128/JVI.03156-15" target="_blank" rel="noreferrer noopener">10.1128/JVI.03156-15</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).
2016
3T3 Cells
Animals
Cardona Sandra M
Cell Line
Cell Proliferation
Cell Survival
Department of Integrative Medical Sciences
Dunphy Jaclyn M
env/biosynthesis
Female
Gene Products
Journal of virology
Leukemia Virus
Li Ying
Lynch Connor R
Lynch William P
Macklin Wendy B
Male
Mice
Motor Neuron Disease/*virology
Murine/*pathogenicity
NEOMED College of Medicine
Neural Stem Cells/*virology
Neurogenesis/*physiology
Neuroglia/*virology
Oligodendroglia/cytology/virology
Pedraza Carlos E
Retroviridae Infections/*complications
Transgenic
-
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/s0168-1702(01)00257-x" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/s0168-1702(01)00257-x</a>
Pages
127–135
Issue
2
Volume
76
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
Changes in BiP (GRP78) levels upon HSV-1 infection are strain dependent.
Publisher
An entity responsible for making the resource available
Virus research
Date
A point or period of time associated with an event in the lifecycle of the resource
2001
2001-08
Subject
The topic of the resource
3T3 Cells; Animals; Carrier Proteins/*biosynthesis/genetics; Heat-Shock Proteins/*biosynthesis/genetics; Herpesvirus 1; Human/isolation & purification/*physiology; Humans; Messenger/metabolism; Mice; Molecular Chaperones/*biosynthesis/genetics; RNA
Creator
An entity primarily responsible for making the resource
Mao H; Palmer D; Rosenthal K S
Description
An account of the resource
BiP (grp78) is a chaperone protein which can also regulate the unfolded protein response of the cell. Levels of BiP increased in cells infected by the small plaque producing, cell associated, neuroinvasive strains of HSV-1 (SP7, 490) but decreased in cells infected with KOS, a large plaque, attenuated strain. BiP protein synthesis continued early in infection and BiP was sequestered and its degradation was limited during SP7 infection. BiP protein synthesis stopped and the protein was degraded in KOS infected cells. These viral strain dependent differences in BiP concentration may influence other aspects of the viral interaction with the target cell and its host.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/s0168-1702(01)00257-x" target="_blank" rel="noreferrer noopener">10.1016/s0168-1702(01)00257-x</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).
2001
3T3 Cells
Animals
Carrier Proteins/*biosynthesis/genetics
Heat-Shock Proteins/*biosynthesis/genetics
Herpesvirus 1
Human/isolation & purification/*physiology
Humans
Mao H
Messenger/metabolism
Mice
Molecular Chaperones/*biosynthesis/genetics
Palmer D
RNA
Rosenthal K S
Virus research
-
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/10.1007/bf02255857" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/bf02255857</a>
Pages
260–266
Issue
4
Volume
5
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
Mice transgenic for simian immunodeficiency virus nef are immunologically compromised.
Publisher
An entity responsible for making the resource available
Journal of biomedical science
Date
A point or period of time associated with an event in the lifecycle of the resource
1998
1998-08
Subject
The topic of the resource
*Genes; *Herpesvirus 1; *Immunocompromised Host; 3T3 Cells; Aging; Animals; Antibodies; Antibody Formation; Cellular; Cercopithecus aethiops; Female; Herpes Simplex/*immunology; HIV/pathogenicity; Human; Humans; Immunity; Immunoglobulin G/blood; Kinetics; Male; Mice; nef; Simian Immunodeficiency Virus/*genetics/pathogenicity; Transgenic; Vero Cells; Viral/biosynthesis/blood
Creator
An entity primarily responsible for making the resource
Larsen N B; Kestler H W; Docherty J J
Description
An account of the resource
An intact nef gene is essential for rapid development of immunodeficiency in human immunodeficiency virus and simian immunodeficiency virus infections. To assess the role of nef in the immune response, mice transgenic for SIV nef were constructed and the humoral and cellular immune response to herpes simplex virus type-1 (HSV-1), measured. Mice transgenic for SIVmac239 nef exhibited a significantly increased mortality rate when challenged with HSV-1 and also showed unusual antibody kinetics in response to viral challenge. During a 32-week period following exposure to HSV, it was noted that IgG subclass titers continued to rise in the nef+ animals, while titers of nef- animals decreased. Additionally, following secondary challenge with HSV, nef- mice had a significantly greater rise in HSV-neutralizing antibody titers than nef+ mice. A decreased proliferative response to the T cell mitogen, PHA, was noted in the nef+ animals. These results suggest that the presence of nef+ is sufficient to induce immune dysfunction.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/bf02255857" target="_blank" rel="noreferrer noopener">10.1007/bf02255857</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).
*Genes
*Herpesvirus 1
*Immunocompromised Host
1998
3T3 Cells
Aging
Animals
Antibodies
Antibody Formation
Cellular
Cercopithecus aethiops
Docherty J J
Female
Herpes Simplex/*immunology
HIV/pathogenicity
Human
Humans
Immunity
Immunoglobulin G/blood
Journal of biomedical science
Kestler H W
Kinetics
Larsen N B
Male
Mice
nef
Simian Immunodeficiency Virus/*genetics/pathogenicity
Transgenic
Vero Cells
Viral/biosynthesis/blood
-
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.24760" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/jcb.24760</a>
Pages
1243–1253
Issue
7
Volume
115
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 promotes osteoblast adhesion through HSPG and alphavbeta1 integrin.
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
2014
2014-07
Subject
The topic of the resource
3T3 Cells; Actin Cytoskeleton/physiology; ADHESION; Alkaline Phosphatase/biosynthesis; Animals; Antibodies/immunology; Cell Adhesion; Cell Differentiation; Cell Line; Cell Proliferation; Chlorates/pharmacology; Extracellular Signal-Regulated MAP Kinases/biosynthesis; Eye Proteins/genetics/immunology/*metabolism; Focal Adhesion Kinase 1/biosynthesis; Focal Adhesions; Heparan Sulfate Proteoglycans/*metabolism; Heparin/pharmacology; Inbred C57BL; INTEGRIN; Membrane Glycoproteins/genetics/immunology/*metabolism; Mice; OSTEOACTIVIN; OSTEOBLAST; OSTEOBLAST DIFFERENTIATION; Osteoblasts/*physiology; Osteogenesis/physiology; Protein Binding; Rats; Receptors; Recombinant Proteins; Vitronectin/immunology/*metabolism
Creator
An entity primarily responsible for making the resource
Moussa Fouad M; Hisijara Israel Arango; Sondag Gregory R; Scott Ethan M; Frara Nagat; Abdelmagid Samir M; Safadi Fayez F
Description
An account of the resource
Osteoactivin (OA), also known as glycoprotein nmb (gpnmb) plays an important role in the regulation of osteoblast differentiation and function. OA induced osteoblast differentiation and function in vitro by stimulating alkaline phosphatase (ALP) activity, osteocalcin production, nodule formation, and matrix mineralization. Recent studies reported a role for OA in cell adhesion and integrin binding. In this study, we demonstrate that recombinant osteoactivin (rOA) as a matricellular protein stimulated adhesion, spreading and differentiation of MC3T3-E1 osteoblast-like cells through binding to alphav beta1 integrin and heparan sulfated proteoglycans (HSPGs). MC3T3-E1 cell adhesion to rOA was blocked by neutralizing anti-OA or anti-alphav and beta1 integrin antibodies. rOA stimulated-osteoblast adhesion was also inhibited by soluble heparin and sodium chlorate. Interestingly, rOA stimulated-osteoblast adhesion promoted an increase in FAK and ERK activation, resulting in the formation of focal adhesions, cell spreading and enhanced actin cytoskeleton organization. In addition, differentiation of primary osteoblasts was augmented on rOA coated-wells marked by increased alkaline phosphatase staining and activity. Taken together, these data implicate OA as a matricellular protein that stimulates osteoblast adhesion through binding to alphav beta1 integrin and cell surface HSPGs, resulting in increased cell spreading, actin reorganization, and osteoblast differentiation with emphasis on the positive role of OA in osteogenesis.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/jcb.24760" target="_blank" rel="noreferrer noopener">10.1002/jcb.24760</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).
2014
3T3 Cells
Abdelmagid Samir M
Actin Cytoskeleton/physiology
ADHESION
Alkaline Phosphatase/biosynthesis
Animals
Antibodies/immunology
Cell Adhesion
Cell Differentiation
Cell Line
Cell Proliferation
Chlorates/pharmacology
Department of Anatomy & Neurobiology
Extracellular Signal-Regulated MAP Kinases/biosynthesis
Eye Proteins/genetics/immunology/*metabolism
Focal Adhesion Kinase 1/biosynthesis
Focal Adhesions
Frara Nagat
Heparan Sulfate Proteoglycans/*metabolism
Heparin/pharmacology
Hisijara Israel Arango
Inbred C57BL
integrin
Journal of cellular biochemistry
Membrane Glycoproteins/genetics/immunology/*metabolism
Mice
Moussa Fouad M
NEOMED College of Medicine
OSTEOACTIVIN
OSTEOBLAST
OSTEOBLAST DIFFERENTIATION
Osteoblasts/*physiology
Osteogenesis/physiology
Protein Binding
Rats
Receptors
Recombinant Proteins
Safadi Fayez F
Scott Ethan M
Sondag Gregory R
Vitronectin/immunology/*metabolism