Porphyromonas endodontalis Lipopolysaccharides Induce RANKL by Mouse Osteoblast in a Way Different from That of Escherichia coli Lipopolysaccharide
Porphyromonas endodontalis Lipopolysaccharides Induce RANKL by Mouse Osteoblast in a Way Different from That of Escherichia coli Lipopolysaccharide
复制标题
牙髓卟啉单胞菌脂多糖通过小鼠成骨细胞诱导 RANKL,其方式与大肠杆菌脂多糖不同
DOI:
10.1016/j.joen.2011.08.015
复制
发表时间:
2011-12-01
影响因子:
4.2
通讯作者:
Zhou, Xuedong
中科院分区:
文献类型:
--
作者:
Tang, Yin;Sun, Feifei;Zhou, Xuedong
Introduction: Porphyromonas endodontalis lipopolysaccharide (LPS) has been shown to have a high positive rate in infected root canals and symptomatic apical periodontitis. It may play an integral role as a potent stimulator of inflammatory cytokines involved in apical lesions. The receptor activator of nuclear factor-kappa B ligand (RANKL) has been proven to be the key regulator of bone remodeling. This study investigated P endodontalis LPS-induced RANKL production and LPS signaling in mouse osteoblasts. Methods: LPS-induced RANKL production in mouse osteoblast MC3T3-E1 cells was measured by Western blot and real-time polymerase chain reaction, and the Toll-like receptors (TLRs) were determined by the blocking test using anti-TLRs antibodies. In addition, specific inhibitors were used to analyze the intracellular signaling pathways. Escherichia coli LPS was used as the control. Results: Both of the anti-TLR2 and anti-TLR4 antibodies significantly (P