Graduate Center for Toxicology, University of Kentucky, Lexington, Kentucky 40536-0001, USA.
BMB Rep. 2010 Jan;43(1):57-61. doi: 10.5483/bmbrep.2010.43.1.057.
Activator protein-1 can induce either cell survival or death, which is controlled by opposing effects of different Jun members. It is generally accepted that c-Jun is pro-apoptotic, but that JunD is anti-apoptotic in stress-exposed cells. Additionally, although there are reports suggesting that JunB plays a protective role, its role in stress-induced apoptosis remains unclear. Here, we investigated the role of JunB in H(2)O(2)-induced cell death using cells that over-expressed the protein or were transfected with si-JunB. Inhibition of JunB expression accelerated H(2)O(2)-mediated loss of mitochondrial membrane potential (MMP) and cytotoxicity. Conversely, over-expression of JunB protein led to significant inhibition of the MMP loss and cell death. The increase in JunB expression also attenuated nuclear relocation of apoptosis-inducing factor and mitochondrial Bcl-2 reduction that occurred following H(2)O(2) exposure. These results suggest that JunB can signal survival against oxidant-mediated cell death by suppressing mitochondrial stress. [BMB reports 2010; 43(1): 57-61].
激活蛋白-1可以诱导细胞存活或死亡，这取决于不同 Jun 成员的相反作用。通常认为 c-Jun 是促凋亡的，但在应激暴露的细胞中 JunD 是抗凋亡的。此外，尽管有报道表明 JunB 发挥保护作用，但它在应激诱导的细胞凋亡中的作用仍不清楚。在这里，我们使用过表达蛋白或转染 si-JunB 的细胞研究了 JunB 在 H2O2 诱导的细胞死亡中的作用。抑制 JunB 的表达加速了 H2O2 介导的线粒体膜电位 (MMP) 和细胞毒性的丧失。相反，JunB 蛋白的过表达导致 MMP 丧失和细胞死亡的显著抑制。JunB 表达的增加也减弱了凋亡诱导因子的核易位和线粒体 Bcl-2 的减少，这些变化发生在 H2O2 暴露之后。这些结果表明 JunB 可以通过抑制线粒体应激来发出信号，以抵抗氧化剂介导的细胞死亡。[BMB 报告 2010;43(1):57-61]。
