Inhibition of tumor progression locus 2 protein kinase decreases lipopolysaccharide-induced tumor necrosis factor α production due to the inhibition of the tip-associated protein induction in RAW264.7 cells
Biological and Pharmaceutical Bulletin, ISSN: 0918-6158, Vol: 33, Issue: 7, Page: 1233-1237
2010
- 4Citations
- 14Captures
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Metrics Details
- Citations4
- Citation Indexes4
- CrossRef4
- Captures14
- Readers14
- 14
Article Description
The activation of mitogen-activated protein kinases (MAPKs) is critically involved in inflammatory events through mediation of the production of various inflammatory cytokines. The Tpl2 (tumor progression locus 2)- MEK (MAPK/ERK kinase)-ERK (extracellular signal-regulated kinase) signaling pathway plays an essential role in the production of tumor necrosis factor α (TNFα) in macrophages stimulated with lipopolysaccharide (LPS). Here, we studied the molecular mechanisms of Tpl2-mediated TNFα production using a potent Tpl2 kinase inhibitor, 1,7-naphtyridine-3-carbonitrile, and LPS-stimulated RAW264.7 cells. This inhibitor was effective in suppressing the in vitro Tpl2 kinase activity, and caused a significant reduction in TNFα production via specific suppression of the phosphorylation of MEK and ERK but not that of p38 and c-Jun N-terminal kinase (JNK). A p38 inhibitor, SB203580, also inhibited the TNFα production dose-dependently. Although the TNFα mRNA level was not altered by either inhibitor, the Tpl2 inhibitor increased the nuclear TNFα mRNA level, while decreasing that in the cytoplasm. Tip-associated protein (TAP), a key molecule in the nucleocytoplasmic transport of TNFα mRNA, was up-regulated by LPS, but this increase was impaired by the Tpl2 inhibitor. In all cases, SB203580 was without effect in the presence of LPS. These results suggest that the LPS-induced TNFα production via the Tpl2-MEK-ERK signaling pathway is regulated by changing the TAP level at the nucleocytoplasmic transport level. These results improve understanding of TNFα regulatory mechanisms and might provide a new therapeutic strategy against inflammatory diseases. © 2010 Pharmaceutical Society of Japan.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=77954508216&origin=inward; http://dx.doi.org/10.1248/bpb.33.1233; http://www.ncbi.nlm.nih.gov/pubmed/20606319; http://www.jstage.jst.go.jp/article/bpb/33/7/33_7_1233/_article; https://dx.doi.org/10.1248/bpb.33.1233; https://www.jstage.jst.go.jp/article/bpb/33/7/33_7_1233/_article; https://www.jstage.jst.go.jp/article/bpb/33/7/33_7_1233/_article/-char/en/; https://www.jstage.jst.go.jp/article/bpb/33/7/33_7_1233/_article/-char/ja/
Pharmaceutical Society of Japan
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