1
40
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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.M501069200" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/jbc.M501069200</a>
Pages
31156–31165
Issue
35
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
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Multiple signals induce endoplasmic reticulum stress in both primary and immortalized chondrocytes resulting in loss of differentiation, impaired cell growth, and apoptosis.
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
2005-09
Subject
The topic of the resource
Animals; Annexin A5/metabolism; Anti-Bacterial Agents/metabolism; Apoptosis/*physiology; Biomarkers; Caspase 12; Caspases/metabolism; CCAAT-Enhancer-Binding Proteins/metabolism; Cell Differentiation/*physiology; Cells; Chondrocytes/cytology/*physiology; Collagen Type II/metabolism; Cultured; DNA Fragmentation; Endoplasmic Reticulum/*metabolism; Extracellular Matrix/metabolism; Gene Expression Regulation; Glucose/metabolism; Proliferating Cell Nuclear Antigen/metabolism; Rats; Signal Transduction/*physiology; Thapsigargin/metabolism; Transcription Factor CHOP; Transcription Factors/metabolism; Tunicamycin/metabolism
Creator
An entity primarily responsible for making the resource
Yang Ling; Carlson Sara G; McBurney Denise; Horton Walter E Jr
Description
An account of the resource
The endoplasmic reticulum is the site of synthesis and folding of secretory proteins and is sensitive to changes in the internal and external environment of the cell. Both physiological and pathological conditions may perturb the function of the endoplasmic reticulum, resulting in endoplasmic reticulum stress. The chondrocyte is the only resident cell found in cartilage and is responsible for synthesis and turnover of the abundant extracellular matrix and may be sensitive to endoplasmic reticulum stress. Here we report that glucose withdrawal, tunicamycin, and thapsigargin induce up-regulation of GADD153 and caspase-12, two markers of endoplasmic reticulum stress, in both primary chondrocytes and a chondrocyte cell line. Other agents such as interleukin-1beta or tumor necrosis factor alpha induced a minimal or no induction of GADD153, respectively. The endoplasmic reticulum stress resulted in decreased chondrocyte growth based on cell counts, up-regulation of p21, and decreased PCNA expression. In addition, perturbation of endoplasmic reticulum function resulted in decreased accumulation of an Alcian Blue positive matrix by chondrocytes and decreased expression of type II collagen at the protein level. Further, quantitative real-time PCR was used to demonstrate a down-regulation of steady state mRNA levels coding for aggrecan, collagen II, and link protein in chondrocytes exposed to endoplasmic reticulum stress-inducing conditions. Ultimately, endoplasmic reticulum stress resulted in chondrocyte apoptosis, as evidenced by DNA fragmentation and annexin V staining. These findings have potentially important implications regarding consequences of endoplasmic reticulum stress in cartilage biology.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1074/jbc.M501069200" target="_blank" rel="noreferrer noopener">10.1074/jbc.M501069200</a>
Rights
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2005
Animals
Annexin A5/metabolism
Anti-Bacterial Agents/metabolism
Apoptosis/*physiology
Biomarkers
Carlson Sara G
Caspase 12
Caspases/metabolism
CCAAT-Enhancer-Binding Proteins/metabolism
Cell Differentiation/*physiology
Cells
Chondrocytes/cytology/*physiology
Collagen Type II/metabolism
Cultured
Department of Anatomy & Neurobiology
DNA Fragmentation
Endoplasmic Reticulum/*metabolism
Extracellular Matrix/metabolism
Gene Expression Regulation
Glucose/metabolism
Horton Walter E Jr
McBurney Denise
NEOMED College of Medicine
Proliferating Cell Nuclear Antigen/metabolism
Rats
Signal Transduction/*physiology
Thapsigargin/metabolism
The Journal of biological chemistry
Transcription Factor CHOP
Transcription Factors/metabolism
Tunicamycin/metabolism
Yang Ling
-
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.21328" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/jcb.21328</a>
Pages
786–800
Issue
3
Volume
102
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
A novel role for Bcl-2 associated-athanogene-1 (Bag-1) in regulation of the endoplasmic reticulum stress response in mammalian chondrocytes.
Publisher
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Journal of cellular biochemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2007
2007-10
Subject
The topic of the resource
*Gene Expression Regulation; Animals; Apoptosis; Biological; Cell Proliferation; Chondrocytes/*metabolism/pathology; Collagen Type II/metabolism; DNA-Binding Proteins/*metabolism/physiology; Endoplasmic Reticulum/metabolism; Models; Phenotype; Rats; RNA Interference; Subcellular Fractions/metabolism; Time Factors; Transcription Factors/*metabolism/physiology; Transfection
Creator
An entity primarily responsible for making the resource
Yang Ling; McBurney Denise; Tang Shou-Ching; Carlson Sara G; Horton Walter E Jr
Description
An account of the resource
BAG-1 (Bcl-2 associated athanogene-1) is a multifunctional protein, linking cell proliferation, cell death, protein folding, and cell stress. In vivo, BAG-1 is expressed in growth plate and articular cartilage, and the expression of BAG-1 is decreased with aging. Chondrocytes respond to endoplasmic reticulum (ER) stress with decreased expression of extracellular matrix proteins, and prolonged ER stress leads to chondrocyte apoptosis. Here we demonstrate for the first time that BAG-1 is involved in ER stress-induced apoptosis in chondrocytes. Induction of ER stress through multiple mechanisms all resulted in downregulation of BAG-1 expression. In addition, direct suppression of BAG-1 expression resulted in chondrocyte growth arrest and apoptosis, while stable overexpression of BAG-1 delayed the onset of ER stress-mediated apoptosis. In addition to regulating apoptosis, we also observed decreased expression of collagen type II in BAG-1 deficient chondrocytes. In contrast, overexpression of BAG-1 resulted in increased expression of collagen type II. Moreover, under ER stress conditions, the reduced expression of collagen type II was delayed in chondrocytes overexpressing BAG-1. These results suggest a novel role for BAG-1 in supporting viability and matrix expression of chondrocytes.
Identifier
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<a href="http://doi.org/10.1002/jcb.21328" target="_blank" rel="noreferrer noopener">10.1002/jcb.21328</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
2007
Animals
Apoptosis
Biological
Carlson Sara G
Cell Proliferation
Chondrocytes/*metabolism/pathology
Collagen Type II/metabolism
Department of Anatomy & Neurobiology
DNA-Binding Proteins/*metabolism/physiology
Endoplasmic Reticulum/metabolism
Horton Walter E Jr
Journal of cellular biochemistry
McBurney Denise
Models
NEOMED College of Medicine
Phenotype
Rats
RNA Interference
Subcellular Fractions/metabolism
Tang Shou-Ching
Time Factors
Transcription Factors/*metabolism/physiology
Transfection
Yang Ling