Abstract：
: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-kappaB and inhibited the production of tumour necrosis factor-alpha 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.
journal_name
Immunologyjournal_title
Immunologyauthors
Khuda II,Koide N,Noman AS,Dagvadorj J,Tumurkhuu G,Naiki Y,Komatsu T,Yoshida T,Yokochi Tdoi
10.1111/j.1365-2567.2010.03274.xsubject
Has Abstractpub_date
2010-09-01 00:00:00pages
59-66issue
1eissn
0019-2805issn
1365-2567pii
IMM3274journal_volume
131pub_type
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