Mechanism of the 24-hour rhythm of tumor necrosis factor-alpha formed by onset of rheumatoid arthritis

Hiromichi Yoshimatsu, Fumiyasu Okazaki, Ichiro Ieiri, Hideto To

研究成果: ジャーナルへの寄稿記事

2 引用 (Scopus)

抄録

Objective: Morning stiffness and plasma cytokine levels in rheumatoid arthritis (RA) patients exhibit 24-hour variations. Tumor necrosis factor-α (TNF-α) plays a central role in RA clinical conditions, including the invasion of inflammatory cells, destruction of cartilage, systemic inflammatory response and its levels show a 24-hour rhythm after the onset of RA. In this study, we investigated what cytokines and/or transcriptional factors are involved in the formation of 24-hour variations in TNF-α levels after the onset of RA using MRL/Mpj-Tnfrsf6lpr (MRL/lpr) mice. Method: Blood was drawn at six different times from MRL/lpr mice to measure cytokines, serum amyloid A (SAA), IgG rheumatoid factor (IgG-RF) and corticosterone levels. Cytokine and transcriptional factor levels at the different times were measured in 10-and/or 15-week-old MRL/lpr mice. The promoter activity of TNF-α by lymphotoxins (LTs) was investigated using a dual-luciferase assay. Results: SAA and TNF-α concentrations clearly exhibited 24-hour rhythms with higher levels at the light phase and lower levels at the dark phase after RA crisis. The expression of LT-α and LT-β showed significant 24-hour rhythms in 15-week-old MRL/lpr mice and the phases of LT-α and LT-β levels were antiphase compared with that of TNF-α. AP-1 binding sites were found in LT-α and LT-β promoter regions, and jun mRNA expression corresponded to LT-α and LT-β levels. TNF-α promoter activity was decreased due to the co-transfection of LT-α and LT-β. Conclusion: LT-α and LT-β controls the 24-hour rhythm in TNF-α levels after the onset of RA in order to suppress TNF-α promoter activity.

元の言語英語
ページ(範囲)564-571
ページ数8
ジャーナルChronobiology International
31
発行部数4
DOI
出版物ステータス出版済み - 1 1 2014

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Lymphotoxin-alpha
Rheumatoid Arthritis
Tumor Necrosis Factor-alpha
Cytokines
Serum Amyloid A Protein
Rheumatoid Factor
Transcription Factor AP-1
Corticosterone
Luciferases
Genetic Promoter Regions
Cartilage
Transfection

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

これを引用

Mechanism of the 24-hour rhythm of tumor necrosis factor-alpha formed by onset of rheumatoid arthritis. / Yoshimatsu, Hiromichi; Okazaki, Fumiyasu; Ieiri, Ichiro; To, Hideto.

:: Chronobiology International, 巻 31, 番号 4, 01.01.2014, p. 564-571.

研究成果: ジャーナルへの寄稿記事

Yoshimatsu, Hiromichi ; Okazaki, Fumiyasu ; Ieiri, Ichiro ; To, Hideto. / Mechanism of the 24-hour rhythm of tumor necrosis factor-alpha formed by onset of rheumatoid arthritis. :: Chronobiology International. 2014 ; 巻 31, 番号 4. pp. 564-571.
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abstract = "Objective: Morning stiffness and plasma cytokine levels in rheumatoid arthritis (RA) patients exhibit 24-hour variations. Tumor necrosis factor-α (TNF-α) plays a central role in RA clinical conditions, including the invasion of inflammatory cells, destruction of cartilage, systemic inflammatory response and its levels show a 24-hour rhythm after the onset of RA. In this study, we investigated what cytokines and/or transcriptional factors are involved in the formation of 24-hour variations in TNF-α levels after the onset of RA using MRL/Mpj-Tnfrsf6lpr (MRL/lpr) mice. Method: Blood was drawn at six different times from MRL/lpr mice to measure cytokines, serum amyloid A (SAA), IgG rheumatoid factor (IgG-RF) and corticosterone levels. Cytokine and transcriptional factor levels at the different times were measured in 10-and/or 15-week-old MRL/lpr mice. The promoter activity of TNF-α by lymphotoxins (LTs) was investigated using a dual-luciferase assay. Results: SAA and TNF-α concentrations clearly exhibited 24-hour rhythms with higher levels at the light phase and lower levels at the dark phase after RA crisis. The expression of LT-α and LT-β showed significant 24-hour rhythms in 15-week-old MRL/lpr mice and the phases of LT-α and LT-β levels were antiphase compared with that of TNF-α. AP-1 binding sites were found in LT-α and LT-β promoter regions, and jun mRNA expression corresponded to LT-α and LT-β levels. TNF-α promoter activity was decreased due to the co-transfection of LT-α and LT-β. Conclusion: LT-α and LT-β controls the 24-hour rhythm in TNF-α levels after the onset of RA in order to suppress TNF-α promoter activity.",
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AU - Yoshimatsu, Hiromichi

AU - Okazaki, Fumiyasu

AU - Ieiri, Ichiro

AU - To, Hideto

PY - 2014/1/1

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N2 - Objective: Morning stiffness and plasma cytokine levels in rheumatoid arthritis (RA) patients exhibit 24-hour variations. Tumor necrosis factor-α (TNF-α) plays a central role in RA clinical conditions, including the invasion of inflammatory cells, destruction of cartilage, systemic inflammatory response and its levels show a 24-hour rhythm after the onset of RA. In this study, we investigated what cytokines and/or transcriptional factors are involved in the formation of 24-hour variations in TNF-α levels after the onset of RA using MRL/Mpj-Tnfrsf6lpr (MRL/lpr) mice. Method: Blood was drawn at six different times from MRL/lpr mice to measure cytokines, serum amyloid A (SAA), IgG rheumatoid factor (IgG-RF) and corticosterone levels. Cytokine and transcriptional factor levels at the different times were measured in 10-and/or 15-week-old MRL/lpr mice. The promoter activity of TNF-α by lymphotoxins (LTs) was investigated using a dual-luciferase assay. Results: SAA and TNF-α concentrations clearly exhibited 24-hour rhythms with higher levels at the light phase and lower levels at the dark phase after RA crisis. The expression of LT-α and LT-β showed significant 24-hour rhythms in 15-week-old MRL/lpr mice and the phases of LT-α and LT-β levels were antiphase compared with that of TNF-α. AP-1 binding sites were found in LT-α and LT-β promoter regions, and jun mRNA expression corresponded to LT-α and LT-β levels. TNF-α promoter activity was decreased due to the co-transfection of LT-α and LT-β. Conclusion: LT-α and LT-β controls the 24-hour rhythm in TNF-α levels after the onset of RA in order to suppress TNF-α promoter activity.

AB - Objective: Morning stiffness and plasma cytokine levels in rheumatoid arthritis (RA) patients exhibit 24-hour variations. Tumor necrosis factor-α (TNF-α) plays a central role in RA clinical conditions, including the invasion of inflammatory cells, destruction of cartilage, systemic inflammatory response and its levels show a 24-hour rhythm after the onset of RA. In this study, we investigated what cytokines and/or transcriptional factors are involved in the formation of 24-hour variations in TNF-α levels after the onset of RA using MRL/Mpj-Tnfrsf6lpr (MRL/lpr) mice. Method: Blood was drawn at six different times from MRL/lpr mice to measure cytokines, serum amyloid A (SAA), IgG rheumatoid factor (IgG-RF) and corticosterone levels. Cytokine and transcriptional factor levels at the different times were measured in 10-and/or 15-week-old MRL/lpr mice. The promoter activity of TNF-α by lymphotoxins (LTs) was investigated using a dual-luciferase assay. Results: SAA and TNF-α concentrations clearly exhibited 24-hour rhythms with higher levels at the light phase and lower levels at the dark phase after RA crisis. The expression of LT-α and LT-β showed significant 24-hour rhythms in 15-week-old MRL/lpr mice and the phases of LT-α and LT-β levels were antiphase compared with that of TNF-α. AP-1 binding sites were found in LT-α and LT-β promoter regions, and jun mRNA expression corresponded to LT-α and LT-β levels. TNF-α promoter activity was decreased due to the co-transfection of LT-α and LT-β. Conclusion: LT-α and LT-β controls the 24-hour rhythm in TNF-α levels after the onset of RA in order to suppress TNF-α promoter activity.

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