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      Bacterial lipopolysaccharide induces osteoclast formation in RAW 264.7 macrophage cells.

      Biochemical and Biophysical Research Communications

      Animals, Bone Resorption, metabolism, pathology, Cell Differentiation, drug effects, physiology, Cell Line, Escherichia coli, Lipopolysaccharides, administration & dosage, Macrophages, Mice, Osteoclasts

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          Abstract

          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. MGCs 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)-kappaB ligand (RANKL). TNF-alpha might play a critical role in LPS-induced osteoclast formation in RAW 264.7 cells. Inhibitors of NF-kappaB and stress activated protein kinase (SAPK/JNK) prevented the LPS-induced osteoclast formation. The detailed mechanism of LPS-induced osteoclast formation is discussed.

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          Journal
          17597583
          10.1016/j.bbrc.2007.06.023

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