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- Title
Tumor necrosis factor-α augments lipopolysaccharide-induced suppressor of cytokine signalling 3 (SOCS-3) protein expression by preventing the degradation.
- Authors
Dagvadorj, Jargalsaikhan; Naiki, Yoshikazu; Tumurkhuu, Gantsetseg; Noman, Abu Shadat Mohammod; Iftakhar-E-Khuda, Imtiaz; Komatsu, Takayuki; Koide, Naoki; Yoshida, Tomoaki; Yokochi, Takashi
- Abstract
The regulatory role of tumour necrosis factor-α (TNF-α) on the expression of suppressor of cytokine signalling 3 (SOCS-3) in response to lipopolysaccharide (LPS) was examined using peritoneal macrophages from TNF-α-deficient mice. The LPS-induced SOCS-3 expression was markedly augmented in macrophages from wild-type mice whereas such augmentation was not seen in the cells from TNF-α-deficient mice. However, there was no significant difference in the level of SOCS-3 messenger RNA expression between macrophages from wild-type mice and those from TNF-α-deficient mice. The addition of exogenous TNF-α augmented the LPS-induced SOCS-3 expression in macrophages from TNF-α-deficient mice. The pulse chase analysis suggested augmented degradation of LPS-induced SOCS-3 protein in macrophages from TNF-α-deficient mice. Moreover, MG 132, a 26S proteasome inhibitor, sustained the LPS-induced SOCS-3 expression in those cells. The tyrosine phosphorylation of SOCS-3 was definitely induced in LPS-stimulated macrophages from TNF-α-deficient mice but not wild-type mice. A tyrosine phosphatase inhibitor enhanced the tyrosine phosphorylation of SOCS-3 in wild-type mice and accelerated the degradation. Therefore, it was suggested that TNF-α prevented the degradation of SOCS-3 protein via inhibition of the tyrosine phosphorylation in LPS-stimulated macrophages.
- Subjects
TUMOR necrosis factors; CYTOKINES; GENE expression; ENDOTOXINS; TYROSINE
- Publication
Immunology, 2010, Vol 129, Issue 1, p97
- ISSN
0019-2805
- Publication type
Article
- DOI
10.1111/j.1365-2567.2009.03154.x