Deng Fei-Yan, Liu Yao-Zhong, Li Li-Ming, Jiang Chen, Wu Shan, Chen Yuan, Jiang Hui, Yang Fang, Xiong Ji-Xian, Xiao Peng, Xiao Su-Mei, Tan Li-Jun, Sun Xiao, Zhu Xue-Zhen, Liu Man-Yuan, Lei Shu-Feng, Chen Xiang-Ding, Xie Jing-Yun, Xiao Gary G, Liang Song-Ping, Deng Hong-Wen
Laboratory of Molecular and Statistical Genetics, College of Life Sciences, Hunan Normal University, Hunan, P. R. China.
Proteomics. 2008 Oct;8(20):4259-72. doi: 10.1002/pmic.200700480.
Osteoporosis (OP) is a major public health problem, mainly characterized by low bone mineral density (BMD). Circulating monocytes (CMCs) may serve as progenitors of osteoclasts and produce a wide variety of factors important to bone metabolism. However, the specific action mechanism of CMCs in the pathogenesis of OP is far from clear. We performed a comparative protein expression profiling study of CMCs in Chinese premenopausal females with extremely discordant BMD, identified a total of 38 differentially expressed proteins, and confirmed with Western blotting five proteins: ras suppressor protein1 (RSU1), gelsolin (GSN), manganese-containing superoxide dismutase (SOD2), glutathione peroxidase 1(GPX1), and prolyl 4-hydroxylase beta subunit (P4HB). These proteins might affect CMCs' trans-endothelium, differentiation, and/or downstream osteoclast functions, thus contribute to differential osteoclastogenesis and finally lead to BMD variation. The findings promote our understanding of the role of CMCs in BMD determination, and provide an insight into the pathogenesis of human OP.
骨质疏松症（OP）是一个主要的公共卫生问题，主要特征是骨矿物质密度（BMD）低。循环单核细胞（CMCs）可能作为破骨细胞的祖细胞，并产生多种对骨代谢重要的因子。然而，CMCs在OP发病机制中的具体作用机制尚不清楚。我们对骨密度差异极大的中国绝经前女性的CMCs进行了蛋白质表达谱比较研究，共鉴定出38种差异表达蛋白，并通过蛋白质印迹法证实了5种蛋白：ras抑制蛋白1（RSU1）、凝溶胶蛋白（GSN）、含锰超氧化物歧化酶（SOD2）、谷胱甘肽过氧化物酶1（GPX1）和脯氨酰4-羟化酶β亚基（P4HB）。这些蛋白质可能影响CMCs的跨内皮、分化和/或下游破骨细胞功能，从而导致破骨细胞生成差异，最终导致骨密度变化。这些发现促进了我们对CMCs在骨密度测定中作用的理解，并为人类OP的发病机制提供了见解。
