作者: Ming Gao , Beibei Zhao , Minjun Chen , Yun Liu , Ming Xu
DOI: 10.1016/J.BIOMATERIALS.2017.03.027
关键词: MAPK/ERK pathway 、 Molecular biology 、 K562 cells 、 Signal transduction 、 Long non-coding RNA 、 Protein kinase B 、 Programmed cell death 、 STAT5 、 Oxidative phosphorylation 、 Cell biology 、 Biology
摘要: The biosafety and biological effects of silver nanoparticles (AgNPs) on human health attract increasing concern. Although considerable studies have been performed to reveal the molecular mechanisms responsible for AgNP-induced effects, current understanding mainly focuses oxidative stress-associated signaling pathways activated by Ag particles and/or ions. However, bases underlying activation these stress not thoroughly elucidated yet. In study, we aimed shed light erythroid cells from perspective long noncoding RNAs. We identified a long-noncoding RNA molecule, ODRUL, which was substantially enhanced in K562 responding AgNPs, coupled accelerated cell death. Further, uncovered stress-driven Nrf2 transcriptionally promoted ODRUL expression cells. Downstream Nrf2-ODRUL recognized interact with PI4Kα protein modulate activities its targets AKT JNK. As result, Bcl-2 level negatively regulated PI4K-AKT/JNK under stress, leading Together, our findings unearthed that Nrf2-mediated lncRNA indispensable toxicity through regulation AKT/JNK-Bcl-2 dependent physical interaction PI4Kα. Thus, this study would open new path depict