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SB203580 enhances interleukin-1 receptor antagonist gene expression in IFN-γ-stimulated BV2 microglial cells through a composite nuclear factor-κB/PU.1 binding site

Title
SB203580 enhances interleukin-1 receptor antagonist gene expression in IFN-γ-stimulated BV2 microglial cells through a composite nuclear factor-κB/PU.1 binding site
Authors
Park J.-S.Jung S.-H.Seo H.Kim H.-S.
Ewha Authors
김희선박진선
SCOPUS Author ID
김희선scopus; 박진선scopus
Issue Date
2007
Journal Title
Neuroscience Letters
ISSN
0304-3940JCR Link
Citation
vol. 416, no. 2, pp. 169 - 174
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Interleukin-1 receptor antagonist (IL-1ra) is a naturally occurring antagonist of IL-1α and IL-1β binding to the IL-1 receptors and alleviates various inflammatory reactions. Therefore, the upregulation of IL-1ra expression is important for preventing and/or treating inflammatory diseases including many neurodegenerative diseases. This study found that SB203580, which is generally known as a p38 MAP kinase inhibitor and an anti-inflammatory agent, increased the level of IL-1ra expression in IFN-γ-stimulated BV2 microglial cells. This effect is believed to occur through the inhibition of protein kinase B (PKB), independently of the p38 MAP kinase pathways. Further mechanistic studies using an IL-1ra promoter revealed that a composite NF-κB/PU.1 binding site plays an important role in this SB203580-mediated upregulation of IL-1ra. Considering that IFN-γ is a major stimulator of the innate and adaptive immune responses, the upregulation of anti-inflammatory IL-1ra expression by SB203580 in the IFN-γ-stimulated microglia might provide a new therapeutic modality for various inflammatory diseases of the central nervous system. © 2007 Elsevier Ireland Ltd. All rights reserved.
DOI
10.1016/j.neulet.2007.02.005
Appears in Collections:
의과대학 > 의학과 > Journal papers
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