...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Cellular Physiology >Brain-derived neurotrophic factor protects cementoblasts from serum starvation-induced cell death.
【24h】

Brain-derived neurotrophic factor protects cementoblasts from serum starvation-induced cell death.

机译：脑源性神经营养因子保护成牙骨质细胞从血清starvation-induced细胞死亡。

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

Our previous studies have shown that brain-derived neurotrophic factor (BDNF) enhances bone/cementum-related protein gene expression through the TrkB-c-Raf-ERK1/2-Elk-1 signaling pathway in cementoblasts, which play a critical role in the establishment of a functional periodontal ligament. To clarify how BDNF regulates survival in cementoblasts, we examined its effects on cell death induced by serum starvation in immortalized human cementoblast-like (HCEM) cells. BDNF inhibited the death of HCEM cells. Small-interfering RNA (siRNA) for TRKB, a high affinity receptor for BDNF, and for Bcl-2, countered the BDNF-induced decrease in dead cell number. In addition, LY294002, a PI3-kinase inhibitor; SH-6, an Akt inhibitor; and PDTC, a nuclear factor kappa B (NF-kappaB) inhibitor, but not PD98059, an ERK1/2 inhibitor, abolished the protective effect of BDNF against cell death. BDNF enhanced phosphorylated Akt levels, NF-kappaB activity in the nucleus, Bcl-2 mRNA levels, and mitochondrial membrane potential. The blocking of BDNF's actions by treatment with siRNA in all cases for TRKB and Bcl-2, LY294002, SH-6, and PDTC suppressed the enhancement. These findings provide the first evidence that a TrkB-PI3-kinase-Akt-NF-kappaB-Bcl-2 signaling pathway triggered by BDNF and the subsequent protective effect of BDNF on mitochondrial membrane potential are required to rescue HCEM cells from serum starvation-induced cell death. Furthermore, the survival and increased expression of bone/cementum-related proteins induced by BDNF in HCEM cells occur through different signaling pathways.
机译：我们先前的研究表明,脑源性神经营养因子(BDNF)增强骨/ cementum-related蛋白质基因表达通过TrkB-c-Raf-ERK1/2-Elk-1信号在成牙骨质细胞通路,扮演一个至关重要的在建立一个功能中的作用牙周韧带。调节在成牙骨质细胞生存,我们检查了对血清引起的细胞死亡的影响饥饿在永生的人类cementoblast-like (HCEM)细胞。HCEM细胞的死亡。(siRNA) TRKB,高亲和力受体脑源性神经营养因子和bcl - 2, BDNF-induced反驳道死细胞数量减少。LY294002 pi3激酶抑制剂;抑制剂;(NF-kappaB)抑制剂,但不是PD98059 ERK1/2抑制剂,废除的保护作用脑源性神经营养因子对细胞死亡。磷酸化Akt水平,NF-kappaB活动细胞核、bcl - 2 mRNA水平和线粒体膜电位。动作用siRNA在所有情况下TRKB和bcl - 2、LY294002 SH-6, PDTC隐含的增强。提供的第一个证据通路由BDNF和随后引发的保护BDNF对线粒体的影响膜电位需要救援HCEM细胞血清starvation-induced细胞死亡。此外,生存和增加骨/ cementum-related蛋白质的正常表达引起的脑源性神经营养因子在HCEM细胞发生不同的信号通路。

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