• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of cellular physiology. >YAP1 inhibits the induction of TNF-α-stimulated bone-resorbing mediators by suppressing the NF-kB signaling pathway in MC3T3-E1 cells
【24h】

YAP1 inhibits the induction of TNF-α-stimulated bone-resorbing mediators by suppressing the NF-kB signaling pathway in MC3T3-E1 cells

机译：YAP1抑制肿瘤坏死因子-α的诱导刺激微介质通过抑制NF-kB在MC3T3-E1细胞信号通路

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Yes-associated protein 1 (YAP1), the core downstream effector of the Hippo signaling cascade, was involved in the regulation of osteoblast and osteoclast differentiation and in bone metabolism. However, the regulatory effects and mechanisms of YAP1 on bone-remodeling molecules in osteoblasts under inflammation remain unknown. In this study, YAP1 expression level was downregulated after treatment with inflammatory cytokine tumor necrosis factor-α (TNF-α) in MC3T3-E1 cells. The key osteoclastogenic molecules induced by TNF-a, namely, interleukin-6 and receptor activator of nuclear factor-kB (NF-kB) ligand, were suppressed after lentivirus-induced YAP1 overexpression, which dramatically increased the expression level of osteoprotegerin. Conversely, the expression levels of the above factors showed opposite trends in the YAP1 small interfering RNA and YAP1 inhibitor (verteporfin) group. Mechanistically, YAP1 attenuated the TNF-a-induced activation of the NF-kB signaling pathway as revealed by the reduced expression of phosphorylated-p65 and NF-kB reporter activity and the nuclear translocation of p65. Moreover, the expression level of YAP1 suppressed by TNF-a was reversed by berberine in concentration-dependent manner. Taken together, our study suggests that YAP1 plays a critical role in the regulation of bone metabolism and is a potential therapeutic target for treating inflammatory bone resorption.
机译：Yes-associated蛋白1 (YAP1)的核心河马的下游效应信号级联、参与的规定成骨细胞和破骨细胞分化和骨代谢。和机制YAP1骨重塑分子在成骨细胞炎症仍然未知。水平治疗后表达下调炎性细胞因子肿瘤坏死因子-α在MC3T3-E1细胞(TNF -α)。由TNF-a osteoclastogenic分子诱导,也就是说,白细胞介素- 6和受体激活核factor-kB (NF-kB)配体,抑制后lentivirus-induced YAP1过度,这大大增加了表达水平osteoprotegerin。上述因素的水平显示相反小干扰RNA和YAP1 YAP1的趋势抑制剂(verteporfin)组。YAP1减毒TNF-a-induced激活透露的NF-kB信号通路减少了phosphorylated-p65和的表达式NF-kB记者活动和核p65易位。YAP1水平抑制TNF-a被逆转小檗碱浓度的方式。综上所述,我们的研究表明,YAP1在骨的规定中扮演一个关键的角色新陈代谢,是一个潜在的治疗目标治疗炎症性骨吸收。

著录项

相似文献

  • 外文文献
  • 中文文献
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号