期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 428, 期 1, 页码 110-115出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2012.10.016
关键词
Toll-like receptor 2; TLR2/6 and TLR2/1; Bone resorption; Prostaglandin E; Periodontitis; Osteoblasts
资金
- Grants-in-Aid for Scientific Research [23590069] Funding Source: KAKEN
TLR2 forms heterodimers with TLR1 and TLR6, and regulates host defense mechanisms against pathogens. We examined the role of TLR2 heterodimer signaling in osteoclast formation and inflammatory periodontitis. In co-cultures of mouse bone marrow cells and osteoblasts, a TLR2/6 ligand (diacylated lipopeptide designed from Gram-positive bacteria) markedly induced osteoclast formation. A TLR2/1 ligand (triacylated lipopeptide designed from Gram-negative bacteria) also induced osteoclast formation. The osteoclast formation induced by TLR2/6 and TLR2/1 ligands was completely suppressed by indomethacin. Osteoblasts expressed TLR1, 2, 4, and 6 mRNAs, and both TLR2/6 and TLR2/1 ligands induced the expression of COX-2, mPGES-1, and RANKL mRNA, as well as PGE production in osteoblasts. Both TLR2/6 and TLR2/1 ligands induced the resorption of mandibular alveolar bone in organ cultures, and elicited inflammatory periodontitis in vivo. Therefore, TLR2 heterodimer signaling may play a key role in PGE-mediated inflammatory bone loss in periodontal disease. (C) 2012 Elsevier Inc. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据