| Autor: |
Khuda, Imtiaz I.-E., Koide, Naoki, Noman, Abu S. M., Dagvadorj, Jargalsaikhan, Tumurkhuu, Gantsetseg, Naiki, Yoshikazu, Komatsu, Takayuki, Yoshida, Tomoaki, Yokochi, Takashi |
| Předmět: |
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| Zdroj: |
Immunology; Sep2010, Vol. 131 Issue 1, p59-66, 8p, 2 Black and White Photographs, 4 Graphs |
| Abstrakt: |
Selective Alzheimer disease indicator-1 (seladin-1) is a broadly expressed oxidoreductase and is related to Alzheimer disease, cholesterol metabolism and carcinogenesis. The effect of lipopolysaccharide (LPS) on the expression of seladin-1 was examined using RAW 264.7 macrophage-like cells and murine peritoneal macrophages. Lipopolysaccharide induced the expression of seladin-1 protein and messenger RNA in those macrophages. The seladin-1 expression was also augmented by a series of Toll-like receptor ligands. The LPS augmented the expression of seladin-1 via reactive oxygen species generation and p38 activation. Seladin-1 inhibited LPS-induced activation of p38 but not nuclear factor-κB and inhibited the production of tumour necrosis factor-α in response to LPS. Moreover, seladin-1 inhibited LPS-induced osteoclast formation and enhanced LPS-induced alkaline phosphatase activity. Therefore, it was suggested that seladin-1 might be an LPS-responsible gene product and regulate the LPS-induced inflammatory response negatively. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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