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首页> 外文期刊>Journal of Cellular Physiology >Oxidized low density lipoprotein decreases Rankl-induced differentiation of osteoclasts by inhibition of Rankl signaling.
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Oxidized low density lipoprotein decreases Rankl-induced differentiation of osteoclasts by inhibition of Rankl signaling.

机译：氧化低密度脂蛋白降低Rankl-induced破骨细胞的分化Rankl信号的抑制。

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摘要

The role of OxLDL in the generation and progression of atherosclerosis is well admitted. In addition, it is well known that atherosclerosis is often accompanied by perturbations in bone remodeling, resulting in osteoporosis. In the current studies, the effect of Cu(2+)-oxidized LDL (OxLDL) on RANKL-induced RAW264.7 mouse monocytes-macrophages differentiation to osteoclasts and on RANKL signaling pathway was investigated. OxLDL, within the range of 10-50 microg protein/ml, prevented RANKL-induced generation of multinucleated osteoclast-like cells and RANKL-induced tartrate resistant acid phosphatase (TRAP) activity. OxLDL also prevented the RANKL-induced phosphorylation of ERK, p38 and JNK kinases, together with the RANKL-induced DNA binding activities of NFkappaB and NFAT transcription factors. Concomitantly, OxLDL enhanced RANKL-induced generation of reactive oxygen species in a dose-dependent manner. The antioxidant glutathione (GSH) prevented whereas the prooxidant compound buthionine-sulfoximine (BSO) enhanced the effect of OxLDL on RANKL-induced oxidative stress and RANKL-induced differentiation. Finally, OxLDL also prevented RANKL-induced TRAP activity and RANKL-induced bone resorbing activity of human peripheral blood mononuclear cells. These results demonstrate that OxLDL, by generation of an intracellular oxidative stress, prevents the differentiation of osteoclasts by inhibition of RANKL signaling pathway. This might be related to the fact that atherosclerosis is accompanied by perturbations in bone and vascular remodeling, leading to osteoporosis and vascular calcification.
机译：生成和OxLDL所扮演的角色动脉粥样硬化的进展也承认。此外,众所周知,动脉粥样硬化往往伴随着在骨重塑扰动,导致骨质疏松症。铜(2 +)RANKL-induced氧化低密度脂蛋白(OxLDL)RAW264.7鼠标monocytes-macrophages分化为破骨细胞RANKL信号通路是调查。的范围10 - 50 microg蛋白质/毫升,预防RANKL-induced代的多核osteoclast-like细胞和RANKL-induced酒石酸耐酸性磷酸酶(陷阱)活动。也避免了RANKL-induced磷酸化物和p38激酶ERK,一起RANKL-induced DNA结合NFkappaB活动和NFAT转录因子。OxLDL增强RANKL-induced代活性氧存在剂量依赖的相关性的方式。预防而prooxidant化合物buthionine-sulfoximine (BSO)增强的效果OxLDL RANKL-induced氧化应激和RANKL-induced分化。也避免RANKL-induced活动和陷阱RANKL-induced骨突起的人类活动外周血单核细胞。证明OxLDL,生成的细胞内氧化应激,阻止了通过抑制破骨细胞的分化RANKL信号通路。动脉粥样硬化是伴随着这一事实扰动在骨骼和血管重建,导致骨质疏松和血管钙化。

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