A novel tumor necrosis factor α–responsive CCAAT/enhancer binding protein site regulates expression of the cartilage‐derived retinoic acid–sensitive protein gene in cartilage

Imamura, Toshihiro; Imamura, Chisako; McAlinden, Audrey; Davies, Sherri R.; Iwamoto, Yukihide; Sandell, Linda J.

doi:10.1002/art.23438

Cited by 14 publications

(16 citation statements)

References 47 publications

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“…C/EBP has been shown to regulate a set of chemokines (4,20,21). We have previously shown that C/EBP␤ is associated with IL-1␤-induced and tumor necrosis factor-␣ (TNF-␣)-induced downregulation of matrix genes in chondrocytes and the repression of cartilage gene expression in non-cartilaginous tissues (22)(23)(24)(25). Here, we investigated the roles of C/EBP␤ and NF-B in the up-regulation of two chemokine genes, CCL3 (MIP-1␣; macrophage inflammatory protein 1␣) and CCL4 (MIP-1␤), in human chondrocytes in response to IL-1␤.…”

mentioning

confidence: 99%

CCAAT/Enhancer-binding Protein β and NF-κB Mediate High Level Expression of Chemokine Genes CCL3 and CCL4 by Human Chondrocytes in Response to IL-1β*

Zhang

Bryan²,

DeLassus³

et al. 2010

Journal of Biological Chemistry

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confidence: 99%

CCAAT/Enhancer-binding Protein β and NF-κB Mediate High Level Expression of Chemokine Genes CCL3 and CCL4 by Human Chondrocytes in Response to IL-1β*

Zhang

Bryan²,

DeLassus³

et al. 2010

Journal of Biological Chemistry

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“…In fact, combinatorial transcriptional protein complex formation is considered the basis of spatiotemporal gene regulation (3)(4)(5)(6)(7). Consistent with this, SOX9 associates with cofactors that regulate histone acetylation and deacetylation, which in turn impact the SOX9-dependent transcriptional program (3)(4)(5)(6)(7).…”

Section: Switching Gears To An Arthritis Gene Expression Network By Smentioning

confidence: 80%

“…In general, transcription factors may require transcription cofactors that regulate chromatin via histone modification (e.g., acetylation or methylation) (3)(4)(5)(6)(7). In fact, combinatorial transcriptional protein complex formation is considered the basis of spatiotemporal gene regulation (3)(4)(5)(6)(7). Consistent with this, SOX9 associates with cofactors that regulate histone acetylation and deacetylation, which in turn impact the SOX9-dependent transcriptional program (3)(4)(5)(6)(7).…”

Section: Switching Gears To An Arthritis Gene Expression Network By Smentioning

confidence: 98%

“…While the transcription targets of SOX9 during development and homeostasis have not been fully determined, it is well established that the transcription of cartilage-specific extracellular matrix genes, such as COL2A1, are directly and tightly regulated by SOX9 (1-3). In general, transcription factors may require transcription cofactors that regulate chromatin via histone modification (e.g., acetylation or methylation) (3)(4)(5)(6)(7). In fact, combinatorial transcriptional protein complex formation is considered the basis of spatiotemporal gene regulation (3)(4)(5)(6)(7).…”

Section: Switching Gears To An Arthritis Gene Expression Network By Smentioning

confidence: 99%

“…While SOX9 does not have intrinsic acetylase activity, the various protein complexes that associate with SOX9 provide it with the ability to fine tune the transcription of its target genes (4)(5)(6)(7). This complex formation is tightly regulated by cellular signals and may act as a sensor for cellular status and developmental timing, and it orchestrates the SOX9 gene expression network.…”

Section: Switching Gears To An Arthritis Gene Expression Network By Smentioning

confidence: 99%

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Switching gears to an arthritis gene expression network by SirT1 cleavage

Asahara

2011

Arthritis & Rheumatism

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Resistin induces expression of proinflammatory cytokines and chemokines in human articular chondrocytes via transcription and messenger RNA stabilization

Zhang

Xing

Hensley

et al. 2010

Arthritis & Rheumatism

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Objective To elucidate the effect of resistin on human articular chondrocytes, and generate a picture of their regulation at the transcriptional and post-transcriptional levels. Methods Human articular chondrocytes were cultured with resistin. Changes in gene expression were analyzed at various doses and times. Cells were also treated with the transcriptional inhibitor actinomycin D after resistin treatment, or the nuclear factor kappa B (NF-κB) inhibitor IKK-NBD before resistin treatment. Gene expression was tested by quantitative real-time polymerase chain reaction. Computational analysis for transcription factor binding motifs was performed on the promoter regions of differentially expressed genes. TC28 chondrocytes were transfected with CCL3 and CCL4 promoter constructs, pNF-κB reporter, and NF-κB and CCAAT/enhancer-binding protein β (C/EBPβ) expression vectors with or without resistin. Results Resistin-treated human articular chondrocytes increased the expression of cytokines and chemokines. The mRNAs for MMP-1, MMP-13 and ADAMTS-4 also increased while COL2A1 and aggrecan were down-regulated. Cytokine and chemokine genes could be categorized into three groups according to the pattern of mRNA expression in a 24 h time course. One pattern suggested rapid regulation by mRNA stability. The second and third patterns were consistent with transcriptional regulation. Computational analysis suggested the transcription factors NF-κB and C/EBPβ were involved in the resistin-induced up-regulation. This prediction was confirmed by the co-transfection of NF-κB and C/EBPβ, and IKK-NBD inhibition. Conclusion Resistin has diverse effects on gene expression in human chondrocytes affecting chemokines, cytokines and matrix genes. mRNA stabilization and transcriptional up-regulation are involved in resistin-induced gene expression in human chondrocytes.

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A novel tumor necrosis factor α–responsive CCAAT/enhancer binding protein site regulates expression of the cartilage‐derived retinoic acid–sensitive protein gene in cartilage

Cited by 14 publications

References 47 publications

CCAAT/Enhancer-binding Protein β and NF-κB Mediate High Level Expression of Chemokine Genes CCL3 and CCL4 by Human Chondrocytes in Response to IL-1β*

CCAAT/Enhancer-binding Protein β and NF-κB Mediate High Level Expression of Chemokine Genes CCL3 and CCL4 by Human Chondrocytes in Response to IL-1β*

Switching gears to an arthritis gene expression network by SirT1 cleavage

Resistin induces expression of proinflammatory cytokines and chemokines in human articular chondrocytes via transcription and messenger RNA stabilization

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