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  • Title: Regulation of osteoclast differentiation by the redox-dependent modulation of nuclear import of transcription factors.
    Author: Huh YJ, Kim JM, Kim H, Song H, So H, Lee SY, Kwon SB, Kim HJ, Kim HH, Lee SH, Choi Y, Chung SC, Jeong DW, Min BM.
    Journal: Cell Death Differ; 2006 Jul; 13(7):1138-46. PubMed ID: 16224490.
    Abstract:
    This study sought to characterize the reduced glutathione (GSH)/oxidized GSSG ratio during osteoclast differentiation and determine whether changes in the intracellular redox status regulate its differentiation through a RANKL-dependent signaling pathway. A progressive decrease of the GSH/GSSG ratio was observed during osteoclast differentiation, and the phenomenon was dependent on a decrease in total glutathione via downregulation of expression of the gamma-glutamylcysteinyl synthetase modifier gene. Glutathione depletion by L-buthionine-(S,R)-sulfoximine (BSO) was found to inhibit osteoclastogenesis by blocking nuclear import of NF-kappaB and AP-1 in RANKL-propagated signaling and bone pit formation by increasing BSO concentrations in mature osteoclasts. Furthermore, intraperitoneal injection of BSO in mice resulted in an increase in bone density and a decrease of the number of osteoclasts in bone. Conversely, glutathione repletion with either N-acetylcysteine or GSH enhanced osteoclastogenesis. These findings indicate that redox status decreases during osteoclast differentiation and that this modification directly regulates RANKL-induced osteoclastogenesis.
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