Pam3CSK4, a TLR2 Agonist, Induces Osteoclastogenesis in RAW 264.7 Cells
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- YANO Akiko
- Department of Pharmacology, Showa University School of Dentistry Department of Periodontology, Showa University School of Dentistry
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- SUZUKI Keiko
- Department of Pharmacology, Showa University School of Dentistry
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- YAMAMOTO Matsuo
- Department of Periodontology, Showa University School of Dentistry
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- YAMADA Shoji
- Department of Pharmacology, Showa University School of Dentistry
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To clarify whether Pam3CSK4, a TLR2 agonist, induces the differentiation of osteoclasts, we investigated the osteoclastogenesis and gene expression induced by Pam3CSK4 in RAW264.7 monocyte/macrophage cells. We found that 1 μg/ml Pam3CSK4 induced osteoclastogenesis without adding RANKL exogenously, whereas 1 μg/ml LPS (Re mutant), a ligand for TLR4, failed to produce osteoclasts in RAW 264.7 cells. The number of TRAP-positive multinuclear cells in the Pam3CSK4 group (156.2 +/− 26.5 cells/well) was significantly (p<0.01) less than that of 100 ng/ml RANKL (196.5 +/− 32.0 cells/well), which was a positive control. Quantitative real-time RT-PCR analysis showed that i) the gene expression levels of TRAP, cathepsin K and matrix metalloproteinase 9, which are osteoclast differentiation markers, were upregulated (p<0.01) by both RANKL and Pam3CSK4, whereas LPS did not increase gene expression of TRAP or cathepsin K, ii) the expression level of RANK was decreased significantly (p<0.01) by both Pam3CSK4 and LPS, but increased by RANKL, iii) the expression levels of TNFα and IL-6, inflammatory cytokines, were upregulated significantly (p<0.01) by both Pam3CSK4 and LPS and iv) the expression level of RANKL was similar to that of other experimental groups in RAW 264.7 cells (p>0.05). Collectively, these results indicate that Pam3CSK4, but not LPS, induces osteoclastogenesis in RAW 264.7 cells in the absence of exogenous RANKL.
収録刊行物
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- Dental Medicine Research
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Dental Medicine Research 32 (3), 181-188, 2012
昭和大学・昭和歯学会
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詳細情報 詳細情報について
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- CRID
- 1390001205458194432
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- NII論文ID
- 10031141316
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- NII書誌ID
- AA12322983
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- COI
- 1:CAS:528:DC%2BC3sXktVKjs70%3D
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- ISSN
- 2186540X
- 18820719
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- NDL書誌ID
- 024268155
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- 本文言語コード
- en
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- データソース種別
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- IRDB
- NDL
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