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首页> 外文期刊>Journal of Cellular Physiology >Osteoprotegerin decreases human osteoclast apoptosis by inhibiting the TRAIL pathway.
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Osteoprotegerin decreases human osteoclast apoptosis by inhibiting the TRAIL pathway.

机译:Osteoprotegerin减少人类的破骨细胞通过抑制细胞凋亡的途径。

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Osteoprotegerin (OPG) is a secreted decoy receptor that recognizes RANKL, and blocks the interaction between RANK and RANKL, leading to the inhibition of osteoclast differentiation and activation. As OPG is a major inhibitor of bone resorption, we wondered whether OPG could modulate osteoclast survival/apoptosis. Osteoclast apoptosis was evaluated by adding various doses of OPG to human osteoclast cultures obtained from cord blood monocytes. Surprisingly, apoptosis decreased after adding the OPG. We hypothesized that OPG may block its second ligand, TRAIL, which is involved in osteoclast apoptosis. We showed that osteoclasts expressed TRAIL, and that TRAIL levels in the culture medium dose-dependently decreased in presence of OPG, as did the level of activated caspase-8 in osteoclasts. In addition, the expression of TRAIL by osteoclasts was not affected in the presence of OPG. Our findings suggest that OPG inhibits osteoclast apoptosis, at least in part, by binding and thus inhibiting endogenously produced TRAIL in human osteoclast cultures. TRAIL could be an autocrine factor for the regulation of osteoclast survival/apoptosis.
机译:Osteoprotegerin(功能)是一种分泌诱饵受体承认RANKL和街区的交互等级和RANKL之间,导致抑制破骨细胞的分化和激活。功能是一个主要的骨吸收抑制剂,我们想知道功能调节破骨细胞生存/凋亡。通过添加不同剂量的评估功能破骨细胞文化从脐带血中获得单核细胞。后添加的功能。可能会阻止第二配体,小道,这是参与破骨细胞凋亡。破骨细胞表达的小道,小道水平的培养基剂量依赖性减少功能,水平也是如此在破骨细胞激活caspase-8。小道被破骨细胞的表达功能的影响。建议功能抑制破骨细胞凋亡,至少在某种程度上,通过结合,从而抑制从内部产生人类破骨细胞文化。破骨细胞生存和凋亡的调节。

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