Lectin-like oxidized low-density lipoprotein receptor-1 abrogation causes resistance to inflammatory bone destruction in mice, despite promoting osteoclastogenesis in the steady state

Nakayachi, Mai; Ito, Junta; Hayashida, Chiyomi; Ohyama, Yoko; Kakino, Akemi; Okayasu, Mari; Sato, Takuya; Ogasawara, Toru; Kaneda, Toshio; Suda, Naoto; Sawamura, Tatsuya; Hakeda, Yoshiyuki

doi:10.1016/j.bone.2015.02.025

Cited by 12 publications

(13 citation statements)

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“…Osteoclast formation proceeds following an interaction between osteoclast lineage cells and osteoblasts [ 37 , 42 ]. Thus, we examined the effect of sudachitin on osteoclastogenesis in a co-culture of isolated osteoblasts and osteoclast precursors derived from bone marrow cells.…”

Section: Resultsmentioning

confidence: 99%

“…The in vivo LPS-induced inflammatory calvarial bone destruction model was established as previously described [ 37 ]. Eight-week-old male C57BL/6J mice were injected with 100 μg LPS subperiosteally into the calvarial bone daily for 5 days.…”

Section: Methodsmentioning

confidence: 99%

“…Osteoblasts were obtained from the calvariae of 3- to 7-day-old C57BL/6J mice by sequential digestion with 0.1% collagenase/0.2% dispase II in α-MEM, as previously described [ 37 ]. The cells released from the 3 rd -5 th digestion were cultured for expansion in α-MEM/10% FBS and stored in liquid nitrogen as calvaria-derived osteoblasts.…”

Section: Methodsmentioning

confidence: 99%

“…After washing the cells with PBS, the cells were lysed in whole-cell lysis buffer [10 mM sodium phosphate (pH 7.5), 150 mM NaCl, 1% NP-40, 0.5% sodium deoxycholate, 0.1% SDS, 1 mM EDTA, 1 mM p- (aminoethyl)benzenesulfonyl fluoride ( p- ABSF), 10 μg/ml leupeptin, 10 μg/ml pepstatin, and 10 μg/ml aprotinin] at 4°C, as previously described [ 37 ]. The whole-cell lysates were centrifuged at 12,000 × g for 10 min, and the supernatants were used for western blotting analysis.…”

Section: Methodsmentioning

confidence: 99%

“…After blocking with 5% skim milk, the membranes were incubated with the indicated antibodies, followed by a peroxidase-conjugated anti-mouse or anti-rabbit IgG antibody. The immunoreactive proteins were visualized, as previously described [ 37 ].…”

Section: Methodsmentioning

confidence: 99%

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The polymethoxy flavonoid sudachitin suppresses inflammatory bone destruction by directly inhibiting osteoclastogenesis due to reduced ROS production and MAPK activation in osteoclast precursors

et al. 2018

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Inflammatory bone diseases, including rheumatoid arthritis, periodontitis and peri-implantitis, are associated not only with the production of inflammatory cytokines but also with local oxidative status, which is defined by intracellular reactive oxygen species (ROS). Osteoclast differentiation has been reported to be related to increased intracellular ROS levels in osteoclast lineage cells. Sudachitin, which is a polymethoxyflavone derived from Citrus sudachi, possesses antioxidant properties and regulates various functions in mammalian cells. However, the effects of sudachitin on inflammatory bone destruction and osteoclastogenesis remain unknown. In calvaria inflamed by a local lipopolysaccharide (LPS) injection, inflammation-induced bone destruction and the accompanying elevated expression of osteoclastogenesis-related genes were reduced by the co-administration of sudachitin and LPS. Moreover, sudachitin inhibited osteoclast formation in cultures of isolated osteoblasts and osteoclast precursors. However, sudachitin rather increased the expression of receptor activator of NF-κB ligand (RANKL), which is an important molecule triggering osteoclast differentiation, and the mRNA ratio of RANKL/osteoprotegerin that is a decoy receptor for RANKL, in the isolated osteoblasts, suggesting the presence of additional target cells. When osteoclast formation was induced from osteoclast precursors derived from bone marrow cells in the presence of soluble RANKL and macrophage colony-stimulating factor, sudachitin inhibited osteoclastogenesis without influencing cell viability. Consistently, the expression of osteoclast differentiation-related molecules including c-fos, NFATc1, cathepsin K and osteoclast fusion proteins such as DC-STAMP and Atp6v0d2 was reduced by sudachitin. In addition, sudachitin decreased activation of MAPKs such as Erk and JNK and the ROS production evoked by RANKL in osteoclast lineage cells. Our findings suggest that sudachitin is a useful agent for the treatment of anti-inflammatory bone destruction.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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