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TXNIP perform a close role in bone loss of rats and mice during glucocorticoid-induced osteoporosis via the mitochondrial oxidative phosphorylation.

Yu-lin Mo,Wenxiu Lai,Y. Zhong,Zhuoqing Hu,Meigui You,Dongtao Wang,Minqun Du,Pan Wang,Xinyou Wu,Cailing Chen,Huanmin He,Zhimin Gao,Yaping Xu,L. Cui,Yajun Yang

Published 2020 in Life Science

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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