lincRNA-Cox2 regulates NLRP3 inflammasome and autophagy mediated neuroinflammation

• DOI: 10.1038/s41418-018-0105-8
• Publication Date: 2018-04-17T09:39:54Z
• Authors: Zhenyi Xue; Zimu Zhang; Hongkun Liu; Wen Li; Xiangdong Guo; Zhihui Zhang; Ying Liu; Long Jia; Yan Li; Yinghui Ren; Hongwei Yang; Lijuan Zhang; Qi Zhang; Yurong Da; Junwei Hao; Zhi Yao; Rongxin Zhang
• Keywords: TRIF; Pyroptosis; AIM2; Crosstalk

Inflammasome activation plays key roles in host defense, but also contributes to the pathogenesis of auto-inflammatory, and neurodegenerative diseases. As autophagy is connected with both innate adaptive immune systems, autophagic dysfunction closely related inflammation, infection, neurodegeneration. Here we identify that lincRNA-Cox2, previously known as a mediator repression genes expression cells, could bind NF-κB p65 promote its nuclear translocation transcription, modulating inflammasome sensor NLRP3 adaptor ASC. Knockdown lincRNA-Cox2 inhibited prevented lincRNA-Cox2-triggered caspase-1 activation, leading decreased IL-1β secretion weakened TIR-domain-containing adapter-inducing interferon-β (TRIF) cleavage, thereby enhancing TRIF-mediated autophagy. Elucidation link between inflammasome-autophagy crosstalk macrophage microglia reveals role for lncRNAs autophagy, provides new opportunities therapeutic intervention neuroinflammation-dependent