Seladin-1 is a novel lipopolysaccharide (LPS)-responsive gene and inhibits the tumour necrosis factor-α production and osteoclast formation in response to LPS

Imtiaz I.E. Khuda, Naoki Koide, Abu S.M. Noman, Jargalsaikhan Dagvadorj, Gantsetseg Tumurkhuu, Yoshikazu Naiki, Takayuki Komatsu, Tomoaki Yoshida, Takashi Yokochi

研究成果: Article査読

3 被引用数 (Scopus)

抄録

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.

本文言語English
ページ(範囲)59-66
ページ数8
ジャーナルImmunology
131
1
DOI
出版ステータスPublished - 09-2010
外部発表はい

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

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