TXNIP contributes to bone loss via promoting the mitochondrial oxidative phosphorylation during glucocorticoid-induced osteoporosis.

2021 
Abstract Glucocorticoid-induced osteoporosis (GIO) is a common secondary form of osteoporosis, the mechanisms governing this disease related with oxidative stress but not completely clear. The pathogenesis of this disease is related to mitochondrial oxidative stress induced by reactive oxygen species (ROS). Thioredoxin-interacting protein (TXNIP) is an important protein necessary for regulating cellular ROS production and causing oxidative phosphorylation. In this research, we found that silencing the expression of TXNIPin MG63 cells down-regulated the mRNA associated with the mitochondrial oxidative phosphorylation (MOP) signaling pathway. Furthermore, we established Sprague-Dawley rats model of Glucocorticoid-induced osteoporosis and found that the expression of TXNIP was high level in serum and bone. Moreover, we established the TXNIP gene knockout mice model and treated with glucocorticoid, then (isobaric Tags for Relative and Absolute Quantification) iTRAQ method was used to detect the proteomics of bone tissues and analyze the differential proteins among different groups of mice, and simple western blot was used to detect MOP pathway related proteins. We found that TXNIP is involved in the pathogenesis of GIO, and perform a close role in bone loss procedure via the MOP pathway. Besides, knockout of TXNIP can prevent GIO to some extent.
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