Responses to the proinflammatory cytokines interleukin‐1 and tumor necrosis factor α in cells derived from rheumatoid synovium and other joint tissues involve nuclear factor κB–mediated induction of the Ets transcription factor ESE‐1

Grall, Franck; Gu, Xuesong; Tan, Lujian; Cho, Je‐Yoel; Inan, Mehmet Sait; Pettit, Allison R.; Thamrongsak, Usanee; Choy, Bob K.; Manning, Cathy; Akbarali, Yasmin; Zerbini, Luiz F.; Rudders, Susan A.; Goldring, Steven R.; Gravallese, Ellen M.; Oettgen, Peter; Goldring, Mary B.; Libermann, Towia A.

doi:10.1002/art.10942

Cited by 95 publications

(135 citation statements)

References 51 publications

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“…This was tested in chondrocytes by treating cultured cells with the 110-kd fibronectin fragment and the cytokine IL-1␤. Both these factors are found in OA cartilage (14,30) and have been shown to stimulate signaling pathways that result in increased NF-B activity (31,32). Consistent with this, both fibronectin fragments and IL-1␤ stimulated RAGE expression (mean Ϯ SEM 172 Ϯ 18% of control and 185 Ϯ 24% of control, respectively), measured using real-time PCR (Figure 4).…”

supporting

confidence: 67%

Articular chondrocytes express the receptor for advanced glycation end products: Potential role in osteoarthritis

Loeser

Yammani

Carlson

et al. 2005

Arthritis & Rheumatism

209

180

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Objective. The receptor for advanced glycation end products (RAGE) binds multiple ligands, including S100 proteins, high mobility group box chromosomal protein 1 (HMGB-1), and AGEs, all of which are present in articular cartilage. Stimulation of RAGE signaling can lead to MAP kinase activation and increased NF-B activity. The objective of the present study was to determine if chondrocytes express functional RAGE.Methods. The presence of chondrocyte RAGE was analyzed by immunohistochemistry using normal and osteoarthritic (OA) cartilage from young and old monkeys and humans, immunoblotting of chondrocyte lysates and human cartilage extracts, and reverse transcription-polymerase chain reaction (RT-PCR) analysis of RNA from chondrocytes treated with interleukin-1 (IL-1) and fibronectin fragments. RAGE signaling was evaluated by stimulating chondrocytes with S100B and HMGB-1 and analyzing for activation of the ERK MAP kinase and NF-B. The ability of S100B and HMGB-1 to stimulate matrix metalloproteinase 13 (MMP-13) production was also assessed. A pull-down assay using biotin-labeled S100B was used to demonstrate binding to RAGE.Results. RAGE was detected in sections of monkey knee cartilage and human knee and ankle cartilage. Increased immunostaining for RAGE was noted in cartilage from older adult monkeys and humans and was further increased in OA tissue. RAGE was also detected by immunoblotting and by RT-PCR, where IL-1␤ and fibronectin fragments were found to stimulate RAGE expression. Stimulation of chondrocytes with S100B or HMGB-1 increased phosphorylation of the ERK MAP kinase and the p65 subunit of NF-B and increased the production of MMP-13. This signaling was inhibited in cells pretreated with soluble RAGE, and S100B was shown to bind to chondrocyte RAGE.Conclusion. Articular chondrocytes express functional RAGE. The increase in RAGE noted in OA cartilage and the ability of RAGE ligands to stimulate chondrocyte MAP kinase and NF-B activity and to stimulate MMP-13 production suggests that chondrocyte RAGE signaling could play a role in OA.

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supporting

confidence: 67%

Articular chondrocytes express the receptor for advanced glycation end products: Potential role in osteoarthritis

Loeser

Yammani

Carlson

et al. 2005

Arthritis & Rheumatism

209

180

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“…To examine whether ESE-1 and ESE-3 expression in epithelial cells can be induced by IL-1β and/or TNF-α as in non-epithelial cells [23][24][25][26], we stimulated cultured human bronchial epithelial cells (BEAS-2B) with IL-1β and/or TNF-α. Using semi-quantitative RT-PCR (data not shown), we detected increased ESE-1 and ESE-3 but not ESE-2 mRNA expression after cytokine induction.…”

Section: Ese-1 and Ese-3 Are Upregulated In Bronchial Epithelial Cellmentioning

confidence: 99%

“…To examine which NF-κB sites in the ESE-1 and ESE-3 promoters are essential for cytokine induction, we selected the NF-κB sites most proximal to the transcription start sites [25] and performed site-direct mutagenesis. We modified the ESE-1 NF-κB binding site GGA AAT CCCC (position -87 to -78) to GGA AAT CGGA and the ESE-3 NF-κB binding site GGG AAT TCCC (-119 to -110) to GGG AAT TGGA; transfection was performed as above.…”

Section: Nf-κb Is Directly Involved In Inducing Ese-1 and Ese-3 Exprementioning

confidence: 99%

“…The expression of ESE-1 can be induced by inflammatory cytokines (IL-1β and TNF-α) in cultured non-epithelial cells, such as vascular smooth muscle cells, endothelial cells, monocytes [23] and fibroblasts [24,25]. ESE-3 mRNA expression is induced in bronchial smooth muscle cells and fibroblasts and is constitutively expressed in human bronchial epithelial cells [26].…”

Section: Introductionmentioning

confidence: 99%

“…However, it is unknown whether these ESE genes are regulated by cytokines in airway epithelial cells. The induction of ESE-1 expression requires the activation of NF-κB [25]. The NF-κB pathway is one of the most important signaling cascades for the regulation of inflammation, which includes cytokine expression and immune responses [27,28].…”

Section: Introductionmentioning

confidence: 99%

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Regulation of epithelium-specific Ets-like factors ESE-1 and ESE-3 in airway epithelial cells: potential roles in airway inflammation

Duan

Cao

et al. 2008

Cell Res

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Airway inflammation is the hallmark of many respiratory disorders, such as asthma and cystic fibrosis. Changes in airway gene expression triggered by inflammation play a key role in the pathogenesis of these diseases. Genetic linkage studies suggest that ESE-2 and ESE-3, which encode epithelium-specific Ets-domain-containing transcription factors, are candidate asthma susceptibility genes. We report here that the expression of another member of the Ets family transcription factors ESE-1, as well as ESE-3, is upregulated by the inflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in bronchial epithelial cell lines. Treatment of these cells with IL-1β and TNF-α resulted in a dramatic increase in mRNA expression for both ESE-1 and ESE-3. We demonstrate that the induced expression is mediated by activation of the transcription factor NF-κB. We have characterized the ESE-1 and ESE-3 promoters and have identified the NF-κB binding sequences that are required for the cytokine-induced expression. In addition, we also demonstrate that ESE-1 upregulates ESE-3 expression and downregulates its own induction by cytokines. Finally, we have shown that in Elf3 (homologous to human ESE-1) knockout mice, the expression of the inflammatory cytokine interleukin-6 (IL-6) is downregulated. Our findings suggest that ESE-1 and ESE-3 play an important role in airway inflammation.

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Rheumatoid arthritis

Detert

2016

The Human Microbiota and Chronic Disease

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Responses to the proinflammatory cytokines interleukin‐1 and tumor necrosis factor α in cells derived from rheumatoid synovium and other joint tissues involve nuclear factor κB–mediated induction of the Ets transcription factor ESE‐1

Abstract: Conclusion. ESE-1 is expressed in synovial tissues in RA and, to a variable extent, in OA, and is specifically induced in synovial fibroblasts, chondroDr. Libermann

Cited by 95 publications

References 51 publications

Articular chondrocytes express the receptor for advanced glycation end products: Potential role in osteoarthritis

Articular chondrocytes express the receptor for advanced glycation end products: Potential role in osteoarthritis

Regulation of epithelium-specific Ets-like factors ESE-1 and ESE-3 in airway epithelial cells: potential roles in airway inflammation

Rheumatoid arthritis

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