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Text
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URL Address
<a href="http://doi.org/10.1002/jcb.10442" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/jcb.10442</a>
Pages
941–953
Issue
5
Volume
88
Dublin Core
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Title
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Coordinate down-regulation of cartilage matrix gene expression in Bcl-2 deficient chondrocytes is associated with decreased SOX9 expression and decreased mRNA stability.
Publisher
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Journal of cellular biochemistry
Date
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2003
2003-04
Subject
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Aggrecans; Animals; C-Type; Cell Line; Chondrocytes/*physiology; Collagen Type II/genetics/metabolism; Dactinomycin; Down-Regulation; Extracellular Matrix Proteins/analysis/genetics/*metabolism; Gene Expression Regulation; Glycoproteins/analysis/genetics/*metabolism; High Mobility Group Proteins/genetics/*metabolism; Lectins; Matrilin Proteins; Messenger/analysis/biosynthesis; Polymerase Chain Reaction/methods; Proteoglycans/genetics/metabolism; Proto-Oncogene Proteins c-bcl-2/deficiency/genetics/*physiology; Rats; RNA; RNA Stability; Signal Transduction; SOX9 Transcription Factor; Transcription Factors/genetics/*metabolism; Transfection
Creator
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Kinkel Mary D; Horton Walter E Jr
Description
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The anti-apoptotic protein Bcl-2 has been shown to function in roles unrelated to apoptosis in a variety of cell types. We have previously reported that loss of Bcl-2 expression alters chondrocyte morphology and modulates aggrecan expression via an apoptosis-independent pathway. Here we show that Bcl-2 is required for chondrocytes to maintain expression of a variety of cartilage-specific matrix proteins. Using quantitative, real-time PCR, we demonstrate that Bcl-2-deficient chondrocytes coordinately down-regulate genes coding for hyaline cartilage matrix proteins including collagen II, collagen IX, aggrecan, and link protein. The decrease in steady-state level of these mRNA transcripts results, in part, from decreased mRNA stability in Bcl-2-deficient chondrocytes. Transcriptional regulation is also likely involved because chondrocytes with decreased Bcl-2 levels show decreased expression of SOX9, a transcription factor necessary for expressing the major cartilage matrix proteins. In contrast, chondrocytes constitutively expressing Bcl-2 have a stable phenotype when subjected to loss of serum factor signaling. These cells maintain high levels of SOX9, as well as the SOX9 targets collagen II and aggrecan. These results suggest that Bcl-2 is involved in a pathway important for maintaining a stable chondrocyte phenotype.
Identifier
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<a href="http://doi.org/10.1002/jcb.10442" target="_blank" rel="noreferrer noopener">10.1002/jcb.10442</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).
2003
Aggrecans
Animals
C-Type
Cell Line
Chondrocytes/*physiology
Collagen Type II/genetics/metabolism
Dactinomycin
Down-Regulation
Extracellular Matrix Proteins/analysis/genetics/*metabolism
Gene Expression Regulation
Glycoproteins/analysis/genetics/*metabolism
High Mobility Group Proteins/genetics/*metabolism
Horton Walter E Jr
Journal of cellular biochemistry
Kinkel Mary D
Lectins
Matrilin Proteins
Messenger/analysis/biosynthesis
Polymerase Chain Reaction/methods
Proteoglycans/genetics/metabolism
Proto-Oncogene Proteins c-bcl-2/deficiency/genetics/*physiology
Rats
RNA
RNA Stability
Signal Transduction
SOX9 Transcription Factor
Transcription Factors/genetics/*metabolism
Transfection