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/10.1152/jn.00227.2014" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/jn.00227.2014</a>
Pages
683–704
Issue
3
Volume
112
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
Postinhibitory rebound neurons and networks are disrupted in retrovirus-induced spongiform neurodegeneration.
Publisher
An entity responsible for making the resource available
Journal of neurophysiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
2014-08
Subject
The topic of the resource
Action Potentials/physiology; Animals; Antigens/metabolism; auditory midbrain; Calcium/metabolism; env/metabolism; Experimental/physiopathology; Gene Products; Hearing Loss/physiopathology; Inferior Colliculi/physiopathology/virology; inferior colliculus; Leukemia; Leukemia Virus; Membrane Potentials/physiology; Mice; Microglia/physiology/virology; Murine/*physiology; Neural Pathways/physiopathology; Neurodegenerative Diseases/*physiopathology; Neuroglia/physiology/virology; Neurons/*physiology/virology; Patch-Clamp Techniques; postinhibitory rebound neurons; Proteoglycans/metabolism; Retroviridae Infections/*physiopathology/virology; retrovirus; Tissue Culture Techniques; Tumor Virus Infections/*physiopathology/virology; Voltage-Sensitive Dye Imaging; voltage-sensitive dyes
Creator
An entity primarily responsible for making the resource
Li Ying; Davey Robert A; Sivaramakrishnan Shobhana; Lynch William P
Description
An account of the resource
Certain retroviruses induce progressive spongiform motor neuron disease with features resembling prion diseases and amyotrophic lateral sclerosis. With the neurovirulent murine leukemia virus (MLV) FrCasE, Env protein expression within glia leads to postsynaptic vacuolation, cellular effacement, and neuronal loss in the absence of neuroinflammation. To understand the physiological changes associated with MLV-induced spongiosis, and its neuronal specificity, we employed patch-clamp recordings and voltage-sensitive dye imaging in brain slices of the mouse inferior colliculus (IC), a midbrain nucleus that undergoes extensive spongiosis. IC neurons characterized by postinhibitory rebound firing (PIR) were selectively affected in FrCasE-infected mice. Coincident with Env expression in microglia and in glia characterized by NG2 proteoglycan expression (NG2 cells), rebound neurons (RNs) lost PIR, became hyperexcitable, and were reduced in number. PIR loss and hyperexcitability were reversed by raising internal calcium buffer concentrations in RNs. PIR-initiated rhythmic circuits were disrupted, and spontaneous synchronized bursting and prolonged depolarizations were widespread. Other IC neuron cell types and circuits within the same degenerative environment were unaffected. Antagonists of NMDA and/or AMPA receptors reduced burst firing in the IC but did not affect prolonged depolarizations. Antagonists of L-type calcium channels abolished both bursts and slow depolarizations. IC infection by the nonneurovirulent isogenic virus Friend 57E (Fr57E), whose Env protein is structurally similar to FrCasE, showed no RN hyperactivity or cell loss; however, PIR latency increased. These findings suggest that spongiform neurodegeneration arises from the unique excitability of RNs, their local regulation by glia, and the disruption of this relationship by glial expression of abnormal protein.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/jn.00227.2014" target="_blank" rel="noreferrer noopener">10.1152/jn.00227.2014</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
Action Potentials/physiology
Animals
Antigens/metabolism
auditory midbrain
Calcium/metabolism
Davey Robert A
Department of Integrative Medical Sciences
env/metabolism
Experimental/physiopathology
Gene Products
Hearing Loss/physiopathology
Inferior Colliculi/physiopathology/virology
inferior colliculus
Journal of neurophysiology
Leukemia
Leukemia Virus
Li Ying
Lynch William P
Membrane Potentials/physiology
Mice
Microglia/physiology/virology
Murine/*physiology
NEOMED College of Medicine
Neural Pathways/physiopathology
Neurodegenerative Diseases/*physiopathology
Neuroglia/physiology/virology
Neurons/*physiology/virology
Patch-Clamp Techniques
postinhibitory rebound neurons
Proteoglycans/metabolism
Retroviridae Infections/*physiopathology/virology
retrovirus
Sivaramakrishnan Shobhana
Tissue Culture Techniques
Tumor Virus Infections/*physiopathology/virology
Voltage-Sensitive Dye Imaging
voltage-sensitive dyes
-
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.M502751200" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/jbc.M502751200</a>
Pages
30517–30525
Issue
34
Volume
280
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
Bcl-2 positively regulates Sox9-dependent chondrocyte gene expression by suppressing the MEK-ERK1/2 signaling pathway.
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
2005
2005-08
Subject
The topic of the resource
*Gene Expression Regulation; Adenoviridae/genetics; Animals; Apoptosis; beta-Galactosidase/metabolism; Blotting; Butadienes/pharmacology; Caspase Inhibitors; Cell Differentiation; Cell Line; Chondrocytes/*metabolism; Collagen Type II/metabolism; Down-Regulation; Enzyme Inhibitors/pharmacology; Fibroblasts/metabolism; Fluorescence; Genetic; High Mobility Group Proteins/*metabolism; Lac Operon; Luciferases/metabolism; MAP Kinase Kinase Kinases/*metabolism; Messenger/metabolism; Microscopy; Mitogen-Activated Protein Kinase 1/*metabolism; Mitogen-Activated Protein Kinase 3/*metabolism; NF-kappa B/metabolism; Nitriles/pharmacology; Phenotype; Phosphorylation; Promoter Regions; Protein Kinase C-alpha; Protein Kinase C/antagonists & inhibitors; Proteoglycans/metabolism; Proto-Oncogene Proteins c-bcl-2/*metabolism; Rats; Reverse Transcriptase Polymerase Chain Reaction; RNA; Signal Transduction; Small Interfering/metabolism; SOX9 Transcription Factor; Sprague-Dawley; Time Factors; Transcription; Transcription Factors/*metabolism; Transfection; Western
Creator
An entity primarily responsible for making the resource
Yagi Rieko; McBurney Denise; Horton Walter E Jr
Description
An account of the resource
Bcl-2 is an anti-apoptotic protein that has recently been shown to regulate other cellular functions. We previously reported that Bcl-2 regulates chondrocyte matrix gene expression, independent of its anti-apoptotic function. Here, we further investigate this novel function of Bcl-2 and examine three intracellular signaling pathways likely to be associated with this function. The present study demonstrates that the activity of Sox9, a master transcription factor that regulates the gene expression of chondrocyte matrix proteins, is suppressed by Bcl-2 small interference RNA in the presence of caspase inhibitors. This effect was attenuated by prior exposure of chondrocytes to an adenoviral vector expressing sense Bcl-2. In addition, the down-regulation of Bcl-2, Sox9, and chondrocyte-specific gene expression by serum withdrawal in primary chondrocytes was reversed by expressing Bcl-2. Inhibition of the protein kinase C alpha and NFkappaB pathways had no effect on the maintenance of Sox9-dependent gene expression by Bcl-2. In contrast, whereas the MEK-ERK1/2 pathway negatively regulated the differentiated phenotype in wild type chondrocytes, inhibition of this pathway reversed the loss of differentiation markers and fibroblastic phenotype in Bcl-2-deficient chondrocytes. In conclusion, the present study identifies a specific signaling pathway, namely, MEK-ERK1/2, that is downstream of Bcl-2 in the regulation of Sox9-dependent chondrocyte gene expression and phenotype.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1074/jbc.M502751200" target="_blank" rel="noreferrer noopener">10.1074/jbc.M502751200</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).
*Gene Expression Regulation
2005
Adenoviridae/genetics
Animals
Apoptosis
beta-Galactosidase/metabolism
Blotting
Butadienes/pharmacology
Caspase Inhibitors
Cell Differentiation
Cell Line
Chondrocytes/*metabolism
Collagen Type II/metabolism
Department of Anatomy & Neurobiology
Down-Regulation
Enzyme Inhibitors/pharmacology
Fibroblasts/metabolism
Fluorescence
Genetic
High Mobility Group Proteins/*metabolism
Horton Walter E Jr
Lac Operon
Luciferases/metabolism
MAP Kinase Kinase Kinases/*metabolism
McBurney Denise
Messenger/metabolism
Microscopy
Mitogen-Activated Protein Kinase 1/*metabolism
Mitogen-Activated Protein Kinase 3/*metabolism
NEOMED College of Medicine
NF-kappa B/metabolism
Nitriles/pharmacology
Phenotype
Phosphorylation
Promoter Regions
Protein Kinase C-alpha
Protein Kinase C/antagonists & inhibitors
Proteoglycans/metabolism
Proto-Oncogene Proteins c-bcl-2/*metabolism
Rats
Reverse Transcriptase Polymerase Chain Reaction
RNA
Signal Transduction
Small Interfering/metabolism
SOX9 Transcription Factor
Sprague-Dawley
The Journal of biological chemistry
Time Factors
Transcription
Transcription Factors/*metabolism
Transfection
Western
Yagi Rieko
-
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.ajpath.2016.06.010" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.ajpath.2016.06.010</a>
Pages
2701–2708
Issue
10
Volume
186
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
Histone Deacetylase Inhibitor Vorinostat (SAHA) Suppresses IL-1beta-Induced Matrix Metallopeptidase-13 Expression by Inhibiting IL-6 in Osteoarthritis Chondrocyte.
Publisher
An entity responsible for making the resource available
The American journal of pathology
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-10
Subject
The topic of the resource
Aged; Articular/drug effects/metabolism; Blotting; Cartilage; Chondrocytes/drug effects; Collagen Type II/drug effects/metabolism; Down-Regulation/drug effects; Female; Gene Expression Regulation/*drug effects; Histone Deacetylase Inhibitors/*pharmacology; Humans; Hydroxamic Acids/*pharmacology; Interleukin-1beta/*antagonists & inhibitors/genetics/metabolism; Knee Joint/metabolism; Male; Matrix Metalloproteinase 13/*drug effects/metabolism; Middle Aged; Osteoarthritis/*drug therapy; Proteoglycans/metabolism; Tumor Necrosis Factor-alpha/drug effects/metabolism; Vorinostat; Western
Creator
An entity primarily responsible for making the resource
Makki Mohammad Shahidul; Haqqi Tariq M
Description
An account of the resource
Osteoarthritis (OA) is the most common whole-joint disease and is characterized by progressive loss of the cartilage matrix. Matrix metallopeptidase-13 (MMP-13) is a highly active and an abundantly expressed protease in OA cartilage and chondrocytes and degrades type II collagen and proteoglycans. We investigated the mechanism of MMP-13 suppression by histone deacetylase inhibitor vorinostat (SAHA). OA chondrocytes were obtained from knee cartilage after enzymatic digestion and treated with IL-1beta in the absence or presence of various histone deacetylase inhibitors. Gene expression was quantified using quantitative RT-PCR. Protein expression and chromatin modifications were determined by Western immunoblotting using specific antibodies. The effect of IL-6 on the expression of
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.ajpath.2016.06.010" target="_blank" rel="noreferrer noopener">10.1016/j.ajpath.2016.06.010</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
Aged
Articular/drug effects/metabolism
Blotting
Cartilage
Chondrocytes/drug effects
Collagen Type II/drug effects/metabolism
Department of Anatomy & Neurobiology
Down-Regulation/drug effects
Female
Gene Expression Regulation/*drug effects
Haqqi Tariq M
Histone Deacetylase Inhibitors/*pharmacology
Humans
Hydroxamic Acids/*pharmacology
Interleukin-1beta/*antagonists & inhibitors/genetics/metabolism
Knee Joint/metabolism
Makki Mohammad Shahidul
Male
Matrix Metalloproteinase 13/*drug effects/metabolism
Middle Aged
NEOMED College of Medicine
Osteoarthritis/*drug therapy
Proteoglycans/metabolism
The American journal of pathology
Tumor Necrosis Factor-alpha/drug effects/metabolism
Vorinostat
Western
-
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/ar.21095" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/ar.21095</a>
Pages
775–785
Issue
5
Volume
293
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
Murine metapodophalangeal sesamoid bones: morphology and potential means of mineralization underlying function.
Publisher
An entity responsible for making the resource available
Anatomical record (Hoboken, N.J. : 2007)
Date
A point or period of time associated with an event in the lifecycle of the resource
2010
2010-05
Subject
The topic of the resource
Aging/physiology; Animal Structures; Animals; Biomechanical Phenomena; Bone Development/*physiology; Calcification; Collagen Type II/metabolism; Electron; Extracellular Matrix/metabolism/ultrastructure; Fibrocartilage/physiology/ultrastructure; Forelimb/*anatomy & histology/diagnostic imaging/growth & development; Hindlimb/*anatomy & histology/diagnostic imaging/growth & development; Mice; Microscopy; Movement/physiology; Muscle; Physiologic/*physiology; Proteoglycans/metabolism; Radiography; Sesamoid Bones/*cytology/diagnostic imaging/growth & development; Skeletal/anatomy & histology/physiology; Species Specificity; Tendons/physiology/ultrastructure; Transmission
Creator
An entity primarily responsible for making the resource
Doherty Alison H; Lowder Elizabeth M; Jacquet Robin D; Landis William J
Description
An account of the resource
Normal murine metapodophalangeal sesamoid bones, closely associated with tendons, were examined in terms of their structure and mineralization with reference to their potential function following crystal deposition. This study utilized radiography, whole mount staining, histology, and conventional electron microscopy to establish a maturation timeline of mineral formation in 1- to
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/ar.21095" target="_blank" rel="noreferrer noopener">10.1002/ar.21095</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).
2010
Aging/physiology
Anatomical record (Hoboken, N.J. : 2007)
Animal Structures
Animals
Biomechanical Phenomena
Bone Development/*physiology
Calcification
Collagen Type II/metabolism
Doherty Alison H
Electron
Extracellular Matrix/metabolism/ultrastructure
Fibrocartilage/physiology/ultrastructure
Forelimb/*anatomy & histology/diagnostic imaging/growth & development
Hindlimb/*anatomy & histology/diagnostic imaging/growth & development
Jacquet Robin D
Landis William J
Lowder Elizabeth M
Mice
Microscopy
Movement/physiology
Muscle
Physiologic/*physiology
Proteoglycans/metabolism
Radiography
Sesamoid Bones/*cytology/diagnostic imaging/growth & development
Skeletal/anatomy & histology/physiology
Species Specificity
Tendons/physiology/ultrastructure
Transmission