CDDO-Me, Sulforaphane and tBHQ attenuate the RANKL-induced osteoclast differentiation via activating the NRF2-mediated antioxidant response
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چکیده
منابع مشابه
MafB negatively regulates RANKL-mediated osteoclast differentiation.
Receptor activator of nuclear factor kappaB ligand (RANKL) induces osteoclast formation from hematopoietic cells via regulation of various transcription factors. Here, we show that MafB negatively regulates RANKL-induced osteoclast differentiation. Expression levels of MafB are significantly reduced by RANKL during osteoclastogenesis. Overexpression of MafB in bone marrow-derived monocyte/macro...
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Osteoclast maturation and function primarily depend on receptor activator of NF-κB ligand (RANKL)-mediated induction of nuclear factor of activated T cells c1 (NFATc1), which is further activated via increased intracellular calcium ([Ca(2+)](i)) oscillation. However, the coordination mechanism that mediates Ca(2+) oscillation during osteoclastogenesis remains ill defined. Here, we identified tr...
متن کاملNotch is activated in RANKL-induced osteoclast differentiation and resorption.
The process of osteoclast differentiation and resorption is fine-tuned by signal pathways, which need to be further elucidated. The aim of this study was to explore the possible connections between NF-kappaB and Notch in RANKL-induced osteoclast activity. To this end, RANKL was used to stimulate mouse osteoclast precursor cell line RAW264.7. The number of multinucleated TRAP+ osteoclasts was co...
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Exposure to arsenic is associated with an increased risk of lung disease. Novel strategies are needed to reduce the adverse health effects associated with arsenic exposure in the lung. Nrf2, a transcription factor that mediates an adaptive cellular defense response, is effective in detoxifying environmental insults and prevents a broad spectrum of diseases induced by environmental exposure to h...
متن کاملTransmembrane protein 173 inhibits RANKL-induced osteoclast differentiation.
Tmem173 was identified as a growth inhibitor associated with major histocompatibility complex (MHC) class II and a potential stimulator for IFN-β, an innate immune inducer and a negative feedback controller for RANKL-induced osteoclast differentiation of monocytic macrophage cells. In this study, we confirmed that transmembrane protein 173 (Tmem173) overexpression inhibited the expression of os...
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ژورنال
عنوان ژورنال: Biochemical and Biophysical Research Communications
سال: 2019
ISSN: 0006-291X
DOI: 10.1016/j.bbrc.2019.02.095