核因子κB受体活化因子配体联合巨噬细胞集落刺激因子诱导破骨细胞分化过程中的蛋白-蛋白相互作用网络的研究

摘要

Objective To systemically investigate receptor activator of nuclear factor -kB ligand (RANKL) and macrophage colony-stimulating factor (M-CSF) induced differentiation of osteoclasts. Methods Mouse protein-protein interaction (PPI) database NIA and published microarray dataset GES16749 were used to construct and analyze PPI network of RANKL and M-CSF induced mouse monocyte RAW264.7. Results In the PPI network, transforming growth factor beta receptor 1CTGFBR1), Rous sarcoma oncogene (SRC), myelocytomatosis oncogene (MYC) and integrin beta 3 GTGB3) were able to interact with more proteins and they were the key nodes in the signaling transduction. Con-clusion TGFBR1, SRC, MYC and ITGB3 might be the key points of RANKL and M-CSF induced differentiation of osteoclasts.%目的 系统地认识核因子KB受体活化因子配体(RANKL)联合巨噬细胞集落刺激因子(M-CSF)诱导破骨细胞分化成熟过程中的分子机制.方法 利用小鼠蛋白-蛋白相互作用数据库NIA和公共基因芯片数据GES16749,构建并分析了RANKL联合M-CSF诱导小鼠单核细胞系RAW264.7分化成熟过程的蛋白-蛋白相互作用网络.结果 在蛋白-蛋白相互作用网络中,转化生长因子β受体Ⅰ (TGFBR1)、劳氏肉瘤原癌基因(SRC)、髓细胞增生原癌基因(MYC)和整合素β3 (ITGB3)能够和多种蛋白质分子发生相互作用,是信号在网络中传导的重要承载分子.结论 TGFBR1、SRC、MYC和ITGB3可能是RANKL联合M-CSF诱导破骨细胞发育过程中的关键分子.