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首页> 外文期刊>Journal of Cellular Physiology >Regulation of Osteoblast Migration Involving Receptor Activator of Nuclear Factor-kappa B (RANK) Signaling
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Regulation of Osteoblast Migration Involving Receptor Activator of Nuclear Factor-kappa B (RANK) Signaling

机译：调节成骨细胞迁移涉及受体激活核Factor-kappa B(排名)信号

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Bone remodeling requires osteoclast activation, resorption, and reversal, prior to osteoblast migration into the bone pit. The Receptor Activator of NF-kB (RANK) signaling pathway plays an important role in bone remodeling. Two components of the RANK signaling pathway, RANK Ligand (RANKL) and the decoy receptor Osteoprotegerin (OPG), are expressed predominantly on the surface of osteoblasts, while RANK is principally expressed on the surface of osteoclasts. However, RANK has also been reported to be expressed on the surface of osteoblasts and osteosarcoma tumor cells. Treatment with soluble RANKL (sRANKL) of both normal osteoblasts and osteosarcoma tumor cells activated phosphorylation of ERK, p38(MAPK), Akt, and p65(NF-kappa B). However, modified Boyden chamber assays and wound repair assays showed differential response to sRANKL-induced chemotactic migration in normal osteoblasts and osteosarcoma tumor cells. In contrast to previously published results, both normal osteoblasts and osteosarcoma tumor cells responded to sRANKL-induced chemotactic migration but the normal osteoblasts did so only in the presence of an ERK pathway inhibitor. For both normal and tumor cells, the chemotactic response could be blocked by inhibiting the PI3K/Akt or p65(NF-kappa B) pathway. Response to sRANKL in normal and tumor cells suggests a role for RANK/ERK-mediated signaling in normal osteoblasts chemotactic migration during bone remodeling that is altered or lost during osteosarcoma tumorigenesis. (C) 2015 Wiley Periodicals, Inc.
机译：骨重建需要破骨细胞活化,吸收,逆转前成骨细胞迁移到骨坑。NF-kB活化剂(排名)信号通路一个重要的角色在骨重塑。组件的信号通路,等级配体(RANKL)和诱饵受体Osteoprotegerin(功能),表达主要表面的成骨细胞,虽然排名主要是表达的破骨细胞的表面。表面的表达造骨细胞和骨肉瘤肿瘤细胞。治疗与可溶性RANKL (sRANKL)正常的成骨细胞和骨肉瘤肿瘤细胞激活ERK的磷酸化,p38 MAPK),一种蛋白激酶,和p65 (nf -κB)。然而,Boyden修改室检测和伤口修复检测显示微分响应sRANKL-induced在正常的成骨细胞和趋化迁移骨肉瘤肿瘤细胞。以前公布的结果,正常造骨细胞和骨肉瘤肿瘤细胞回应sRANKL-induced趋化迁移但这样做只在正常的成骨细胞ERK通路抑制剂的存在。正常和肿瘤细胞趋化现象的反应可以被抑制PI3K / Akt还是p65 (nf -κB)的途径。正常和肿瘤细胞显示的作用排名/ ERK-mediated信号在正常的成骨细胞趋化迁移在骨重塑在骨肉瘤是改变或丢失肿瘤发生。

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