Xie Weiwei, Zheng Wei, Liu Min, Qin Qizhong, Zhao Yunpeng, Cheng Zhi, Guo Fengjin
Department of Cell Biology and Genetics, Core Facility of Development Biology, Chongqing Medical University, Chongqing, 400016, China.
Department of Orthopaedic Surgery, Qilu Hospital, Shandong University, Jinan, 250012, China.
Genes Dis. 2018 Apr 27;5(3):226-234. doi: 10.1016/j.gendis.2018.04.004. eCollection 2018 Sep.
Inflammation is indispensable for host defense, whereas excessive inflammation often develop inflammatory diseases. Autophagy is thought to be engaged in many extracellular stress responses, such as starvation and innate immunity. Thus, autophagy plays an important role in maintaining homeostasis. The purpose of this study was to elucidate the function of BRF1 in the regulation of inflammation and autophagy response in macrophages. We found that BRF1 inhibited the LPS-induced inflammatory factors expression and the autophagy flux in macrophage. Furthermore, inhibition autophagy with 3-MA can attenuate the suppressive effect of BRF1 on LPS-mediated inflammation. In addition, MAPK/ERK signaling pathway was involved in the BRF1 inhibition inflammation and autophagy in macrophages. These findings indicate that BRF1 attenuates LPS-induced inflammatory factors secretion through autophagy, at least in part, through MAPK/ERK signaling pathway.
炎症对于宿主防御不可或缺，而过度炎症往往会引发炎症性疾病。自噬被认为参与许多细胞外应激反应，如饥饿和固有免疫。因此，自噬在维持体内平衡中发挥着重要作用。本研究的目的是阐明BRF1在巨噬细胞炎症和自噬反应调节中的功能。我们发现BRF1抑制巨噬细胞中LPS诱导的炎症因子表达和自噬通量。此外，用3-MA抑制自噬可减弱BRF1对LPS介导炎症的抑制作用。此外，MAPK/ERK信号通路参与了BRF1对巨噬细胞炎症和自噬的抑制作用。这些发现表明，BRF1至少部分通过MAPK/ERK信号通路，通过自噬减弱LPS诱导的炎症因子分泌。
