Abstract |
Osteoblasts produce various types of cytokines under pathological conditions and control osteoclast differentiation. Tumor necrosis factor-α (TNF-α) has been demonstrated to exert complex effects in osteoblasts under local inflammatory conditions, including in periodontal and periapical diseases. Interleukin-34 (IL-34) has been recently identified as a novel regulatory factor for the differentiation and function of osteoclasts. The present study provides the first evidence, to the best of our knowledge, that the expression of IL-34 is induced by TNF-α through nuclear factor-κB (NF-κB) activation in MC3T3-E1 osteoblastic cells. TNF-α induced IL-34 expression in a dose- and time-dependent manner. Immunocytochemistry with an NF-κB antibody demonstrated that NF-κB was mainly localized in the cytoplasm of the untreated MC3T3-E1 cells. Rapid translocation of NF-κB from the cytoplasm to the nucleus was observed in the cells treated with TNF-α for 15 min. Translocation and transcriptional activity of NF-κB were also determined by western blotting and a luciferase reporter assay, respectively. Pretreatment with 100 µM CAPE, an inhibitor of NF-κB, significantly inhibited TNF-α-induced IL-34 expression. These results indicate that TNF-α induces IL-34 expression via NF-κB in osteoblasts.
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Authors | Yaqiong Yu, Di Yang, Lihong Qiu, Hirohiko Okamura, Jiajie Guo, Tatsuji Haneji |
Journal | Molecular medicine reports
(Mol Med Rep)
Vol. 10
Issue 3
Pg. 1371-6
(Sep 2014)
ISSN: 1791-3004 [Electronic] Greece |
PMID | 24970360
(Publication Type: Journal Article)
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Chemical References |
- Interleukins
- NF-kappa B
- Tumor Necrosis Factor-alpha
- interleukin-34, mouse
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Topics |
- 3T3 Cells
- Animals
- Cell Differentiation
(drug effects)
- Cell Nucleus
(drug effects, metabolism)
- Dose-Response Relationship, Drug
- Interleukins
(genetics, metabolism)
- Mice
- NF-kappa B
(genetics, metabolism)
- Osteoblasts
(cytology, drug effects, metabolism)
- Signal Transduction
- Tumor Necrosis Factor-alpha
(pharmacology)
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