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Text
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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
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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
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The Journal of biological chemistry
Date
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2005
2005-09
Subject
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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
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Yang Ling; Carlson Sara G; McBurney Denise; Horton Walter E Jr
Description
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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
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<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