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14 results on '"Kitanaka, Taku"'

2. Interleukin-1β triggers matrix metalloprotease-3 expression through p65/RelA activation in melanoma cells

Author

Nunomura, Junichi, primary, Nakano, Rei, additional, Naruke, Atsuto, additional, Suwabe, Yoko, additional, Nakano, Masumi, additional, Yachiku, Naoya, additional, Kuji, Manami, additional, Sugimura, Mana, additional, Namba, Shinichi, additional, Kitanaka, Taku, additional, Kitanaka, Nanako, additional, Sugiya, Hiroshi, additional, and Nakayama, Tomohiro, additional

Published
2022
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4. Involvement of GLUT1 and GLUT3 in the growth of canine melanoma cells

Author

Suwabe, Yoko, primary, Nakano, Rei, additional, Namba, Shinichi, additional, Yachiku, Naoya, additional, Kuji, Manami, additional, Sugimura, Mana, additional, Kitanaka, Nanako, additional, Kitanaka, Taku, additional, Konno, Tadayoshi, additional, Sugiya, Hiroshi, additional, and Nakayama, Tomohiro, additional

Published
2021
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14. Non-Transcriptional and Translational Function of Canonical NF- κ B Signaling in Activating ERK1/2 in IL-1 β -Induced COX-2 Expression in Synovial Fibroblasts.

Author

Nakano R, Kitanaka T, Namba S, Kitanaka N, Suwabe Y, Konno T, Yamazaki J, Nakayama T, and Sugiya H

Subjects
Animals, Cells, Cultured, Cyclooxygenase 2 genetics, Dogs, Enzyme Activation, Fibroblasts enzymology, Fibroblasts pathology, NF-kappa B genetics, Phosphorylation, Signal Transduction, Synovial Membrane enzymology, Synovial Membrane pathology, Synovitis enzymology, Synovitis pathology, Cyclooxygenase 2 metabolism, Fibroblasts drug effects, Interleukin-1beta toxicity, Mitogen-Activated Protein Kinase 1 metabolism, Mitogen-Activated Protein Kinase 3 metabolism, NF-kappa B metabolism, Synovial Membrane drug effects, Synovitis chemically induced
Abstract

The pro-inflammatory cytokine interleukin 1 β (IL-1 β ) induces the synthesis of prostaglandin E 2 by upregulating cyclooxygenase-2 (COX-2) in the synovial tissue of individuals with autoimmune diseases, such as rheumatoid arthritis (RA). IL-1 β -mediated stimulation of NF- κ B and MAPK signaling is important for the pathogenesis of RA; however, crosstalk(s) between NF- κ B and MAPK signaling remains to be understood. In this study, we established a model for IL-1 β -induced synovitis and investigated the role of NF- κ B and MAPK signaling in synovitis. We observed an increase in the mRNA and protein levels of COX-2 and prostaglandin E 2 release in cells treated with IL-1 β . NF- κ B and ERK1/2 inhibitors significantly reduced IL-1 β -induced COX-2 expression. IL-1 β induced the phosphorylation of canonical NF- κ B complex (p65 and p105) and degradation of I κ B α . IL-1 β also induced ERK1/2 phosphorylation but did not affect the phosphorylation levels of p38 MAPK and JNK. IL-1 β failed to induce COX-2 expression in cells transfected with siRNA for p65, p105, ERK1, or ERK2. Notably, NF- κ B inhibitors reduced IL-1 β -induced ERK1/2 phosphorylation; however, the ERK1/2 inhibitor had no effect on the phosphorylation of the canonical NF- κ B complex. Although transcription and translation inhibitors had no effect on IL-1 β -induced ERK1/2 phosphorylation, the silencing of canonical NF- κ B complex in siRNA-transfected fibroblasts prevented IL-1 β -induced phosphorylation of ERK1/2. Taken together, our data indicate the importance of the non-transcriptional/translational activity of canonical NF- κ B in the activation of ERK1/2 signaling involved in the IL-1 β -induced development of autoimmune diseases affecting the synovial tissue, such as RA., (Copyright © 2020 Nakano, Kitanaka, Namba, Kitanaka, Suwabe, Konno, Yamazaki, Nakayama and Sugiya.)

Published
2020
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