| RRC ID |
42480
|
| 著者 |
Tanaka H, Tanabe N, Shoji M, Suzuki N, Katono T, Sato S, Motohashi M, Maeno M.
|
| タイトル |
Nicotine and lipopolysaccharide stimulate the formation of osteoclast-like cells by increasing macrophage colony-stimulating factor and prostaglandin E2 production by osteoblasts.
|
| ジャーナル |
Life Sci
|
| Abstract |
Several studies have indicated that one of the causes of alveolar bone destruction with periodontitis is lipopolysaccharide (LPS) from the cell wall of Gram-negative bacteria in plaque and that tobacco smoking may be an important risk factor for the development and severity of periodontitis. The present study was undertaken to determine the effect of nicotine and LPS on the expression of macrophage colony-stimulating factor (M-CSF), osteoprotegerin (OPG), and prostaglandin E2 (PGE2) in osteoblasts, and the indirect effect of nicotine and LPS on the formation of osteoclast-like cells. Saos-2 cells were cultured with 10(-3) M nicotine, or 1 or 10 microg/ml LPS and 10(-3) M nicotine, for up to 14 days. The gene and protein expression of M-CSF and OPG were determined using real-time PCR and ELISA, respectively. PGE2 expression was determined using ELISA. The formation of osteoclast-like cells was estimated using tartrate-resistant acid phosphatase (TRAP) staining of osteoclast precursors in culture with conditioned medium from nicotine and LPS-treated Saos-2 cells and the soluble receptor activator of NF-kappaB ligand (RANKL). M-CSF and PGE2 expression increased markedly in cells cultured with nicotine and LPS compared with those cultured with nicotine alone. OPG expression increased in the initial stages of culture with nicotine and LPS but decreased in the later stages of culture. The conditioned medium containing M-CSF and PGE2 produced by nicotine and LPS-treated Saos-2 cells with soluble RANKL increased the TRAP staining of osteoclast precursors compared with that produced by nicotine treatment alone. These results suggest that nicotine and LPS stimulate the formation of osteoclast-like cells via an increase in M-CSF and PGE2 production and that the stimulation is greater than with nicotine treatment alone.
|
| 巻・号 |
78(15)
|
| ページ |
1733-40
|
| 公開日 |
2006-3-6
|
| DOI |
10.1016/j.lfs.2005.08.017
|
| PII |
S0024-3205(05)00994-X
|
| PMID |
16266722
|
| MeSH |
Alkaline Phosphatase / metabolism
Animals
Cell Line, Tumor
Cell Proliferation / drug effects
Dinoprostone / metabolism*
Dose-Response Relationship, Drug
Drug Synergism
Enzyme-Linked Immunosorbent Assay
Escherichia coli / chemistry
Gene Expression / drug effects
Glycoproteins / genetics
Glycoproteins / metabolism
Humans
Lipopolysaccharides / isolation & purification
Lipopolysaccharides / toxicity*
Macrophage Colony-Stimulating Factor / genetics
Macrophage Colony-Stimulating Factor / metabolism*
Mice
Nicotine / toxicity*
Osteoblasts / cytology
Osteoblasts / drug effects*
Osteoblasts / metabolism
Osteoclasts / cytology
Osteoclasts / drug effects*
Osteoclasts / metabolism
Osteoprotegerin
Receptors, Cytoplasmic and Nuclear / genetics
Receptors, Cytoplasmic and Nuclear / metabolism
Receptors, Tumor Necrosis Factor / genetics
Receptors, Tumor Necrosis Factor / metabolism
Reverse Transcriptase Polymerase Chain Reaction
|
| IF |
3.647
|
| 引用数 |
60
|
|
WOS 分野
|
PHARMACOLOGY & PHARMACY
MEDICINE, RESEARCH & EXPERIMENTAL
|
| リソース情報 |
| ヒト・動物細胞 |
|
