Bacterial lipopolysaccharide induces osteoclast formation in RAW 264.7 macrophage cells

被引:130
作者
Islam, Shamima [1 ]
Hassan, Ferdaus [1 ]
Tumurkhuu, Gantsetseg [1 ]
Dagvadorj, Jargalsaikhan [1 ]
Koide, Naoki [1 ]
Naiki, Yoshikazu [1 ]
Mori, Isamu [1 ]
Yoshida, Tomoaki [1 ]
Yokochi, Takashi [1 ]
机构
[1] Aichi Med Univ, Sch Med, Dept Microbiol & Immunol, Nagakute, Aichi 4801195, Japan
关键词
osteoclast; lipopolysaccharide; TNF-alpha; receptor activator of nuclear factor-kappa B ligand (RANKL); Jun-N-terminal kinase 1/2 (JNK1/2); macrophage-colony stimulating factor; tartrate-resistant acid phosphatase (TRAP);
D O I
10.1016/j.bbrc.2007.06.023
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Lipopolysaccharide (LPS) is a potent bone resorbing factor. The effect of LPS on osteoclast formation was examined by using murine RAW 264.7 macrophage cells. LPS-induced the formation of multinucleated giant cells (MGC) in RAW 264.7 cells 3 days after the exposure. NIGCs were positive for tartrate-resistant acid phosphatase (TRAP) activity. Further, MGC formed resorption pits on calcium-phosphate thin film that is a substrate for osteoclasts. Therefore, LPS was suggested to induce osteoclast formation in RAW 264.7 cells. LPS-induced osteoclast formation was abolished by anti-tumor necrosis factor (TNF)-alpha antibody, but not antibodies to macrophage-colony stimulating factor (M-CSF) and receptor activator of nuclear factor (NF)-kappa B ligand (RANKL). TNF-alpha might play a critical role in LPS-induced osteoclast formation in RAW 264.7 cells. Inhibitors of NF-kappa B and stress activated protein kinase (SAPK/JNK) prevented the LPS-induced osteoclast formation. The detailed mechanism of LPS-induced osteoclast formation is discussed. (C) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:346 / 351
页数:6
相关论文
共 31 条
[1]  
AKATSU T, 1989, J BONE MINER RES, V4, P29
[2]  
ANDERSON HC, 1989, LAB INVEST, V60, P320
[3]   Tumor necrosis factor-α induces differentiation of and bone resorption by osteoclasts [J].
Azuma, Y ;
Kaji, K ;
Katogi, R ;
Takeshita, S ;
Kudo, A .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (07) :4858-4864
[4]   SP600125, an anthrapyrazolone inhibitor of Jun N-terminal kinase [J].
Bennett, BL ;
Sasaki, DT ;
Murray, BW ;
O'Leary, EC ;
Sakata, ST ;
Xu, WM ;
Leisten, JC ;
Motiwala, A ;
Pierce, S ;
Satoh, Y ;
Bhagwat, SS ;
Manning, AM ;
Anderson, DW .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (24) :13681-13686
[5]  
Chambers TJ, 2000, J PATHOL, V192, P4
[6]   Requirement for NF-κB in osteoclast and B-cell development [J].
Franzoso, G ;
Carlson, L ;
Xing, LP ;
Poljak, L ;
Shores, EW ;
Brown, KD ;
Leonardi, A ;
Tran, T ;
Boyce, BF ;
Siebenlist, U .
GENES & DEVELOPMENT, 1997, 11 (24) :3482-3496
[7]   CELLULAR DIFFERENCES IN ACID PHOSPHATASE ISOENZYMES IN BONE AND TEETH [J].
HAMMARSTROM, LE ;
HANKER, JS ;
TOVERUD, SU .
CLINICAL ORTHOPAEDICS AND RELATED RESEARCH, 1971, (78) :151-+
[8]   Molecular analysis of RANKL-independent cell fusion of osteoclast-like cells induced by TNF-α, lipopolysaccharide, or peptidoglycan [J].
Hotokezaka, Hitoshi ;
Sakai, Eiko ;
Ohara, Naoya ;
Hotokezaka, Yuka ;
Gonzales, Carmen ;
Matsuo, Ken-ichiro ;
Fujimura, Yuji ;
Yoshida, Noriaki ;
Nakayama, Koji .
JOURNAL OF CELLULAR BIOCHEMISTRY, 2007, 101 (01) :122-134
[9]   Mast cell tumor necrosis factor alpha production is regulated by MEK kinases [J].
Ishizuka, T ;
Terada, N ;
Gerwins, P ;
Hamelmann, E ;
Oshiba, A ;
Fanger, GR ;
Johnson, GL ;
Gelfand, EW .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (12) :6358-6363
[10]   Piceatannol prevents lipopolysaccharide (LPS)-induced nitric oxide (NO) production and nuclear factor (NF)-KB activation by inhibiting IKB kinase (IKK) [J].
Islam, S ;
Hassan, F ;
Mu, MM ;
Ito, H ;
Koide, N ;
Mori, I ;
Yoshida, T ;
Yokochi, T .
MICROBIOLOGY AND IMMUNOLOGY, 2004, 48 (10) :729-736