Osteopontin as a positive regulator in the osteoclastogenesis of arthritis
Osteopontin as a positive regulator in the osteoclastogenesis of arthritis
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DOI：
10.1016/j.bbrc.2004.02.124
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发表时间：
2004-04-09
影响因子：
3.1
通讯作者：
Saeki, Y
中科院分区：
文献类型：
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作者：
Ishii, T;Ohshima, S;Saeki, Y
我们利用胶原诱导关节炎（CIA）研究了骨桥蛋白（OPN）在关节炎破骨细胞生成中的作用。野生型（OPN +/+）小鼠关节炎关节细胞自发形成骨吸收破骨细胞样细胞（OCLs）。核因子κ b配体受体激活因子（RANKL）表达增强，骨保护素（OPG）表达降低。OPG的加入减少了ocl的数量，表明破骨细胞的形成依赖于RANK/RANKL/OPG系统。细胞也大量产生OPN，抗OPN中和抗体抑制OCLs的发展。此外，OPN的加入增加了RANKL的表达，增强了oclc从OPN缺陷（OPN -/-）细胞的分化。OPN与1 α、25-二羟基维生素D-3和地塞米松的联合作用一样，在基质细胞系ST2中也增强了RANKL的表达，降低了OPG的表达。这些结果表明，OPN通过RANK/RANKL/OPG系统在关节炎的破骨细胞生成中起积极调节作用。(C) 2004爱思唯尔公司版权所有。
We examined the role of osteopontin (OPN) in the osteoclastogenesis of arthritis using collagen-induced arthritis (CIA). Cells from arthritic joints of wild-type (OPN +/+) mice spontaneously developed bone-resorbing osteoclast-like cells (OCLs). The cultured cells showed an enhanced expression of receptor activator of nuclear factor kappaB ligand (RANKL) and a decreased expression of osteoprotegerin (OPG). The addition of OPG reduced the number of OCLs, indicating that the osteoclastogenesis depends on the RANK/RANKL/OPG system. The cells also produced OPN abundantly and anti-OPN neutralizing antibodies suppressed the development of OCLs. Moreover, the addition of OPN increased the expression of RANKL and augmented differentiation of OCLs from OPN-deficient (OPN -/-) cells. OPN, like the combination of 1alpha,25-dihydroxyvitamin D-3 and dexamethasone, also enhanced the RANKL expression and decreased OPG expression in a stromal cell line, ST2. These results suggest that OPN acts as a positive regulator in the osteoclastogenesis of arthritis through the RANK/RANKL/OPG system. (C) 2004 Elsevier Inc. All rights reserved.