title: Tumor necrosis factor-α induces interleukin-34 expression through nuclear factor‑κB activation in MC3T3-E1 osteoblastic cells.
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.
authors: Department of Endodontics, School of Stomatology, China Medical University, Shenyang, Liaoning 110002, P.R. China.
authors: Yaqiong
authors: Y
authors: Yu
authors: Department of Endodontics, School of Stomatology, China Medical University, Shenyang, Liaoning 110002, P.R. China.
authors: Di
authors: D
authors: Yang
authors: Department of Endodontics, School of Stomatology, China Medical University, Shenyang, Liaoning 110002, P.R. China.
authors: Lihong
authors: L
authors: Qiu
authors: Department of Histology and Oral Histology, Institute of Health Biosciences, The University of Tokushima Graduate School, Kuramoto, Tokushima 770-8504, Japan.
authors: Hirohiko
authors: H
authors: Okamura
authors: Department of Endodontics, School of Stomatology, China Medical University, Shenyang, Liaoning 110002, P.R. China.
authors: Jiajie
authors: J
authors: Guo
authors: Department of Histology and Oral Histology, Institute of Health Biosciences, The University of Tokushima Graduate School, Kuramoto, Tokushima 770-8504, Japan.
authors: Tatsuji
authors: T
authors: Haneji
mesh_terms: D016475:3T3 Cells; D000818:Animals; D002454:Cell Differentiation / Q000187:drug effects; D002467:Cell Nucleus / Q000187:drug effects / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D007378:Interleukins / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism*; D010006:Osteoblasts / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D015398:Signal Transduction; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
chemical_list: D007378:Interleukins; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; C552364:interleukin-34, mouse