Xu Jingbin, Xu Henggui, Ma Kexin, Wang Yue, Niu Ben, Zhang Li, Li Fasheng
Laboratory Medicine College, Dalian Medical University, Dalian, China.
Department of Central Laboratory, Dalian Municipal Central Hospital Affiliated of Dalian Medical University, Dalian, China.
Front Cell Dev Biol. 2021 Mar 16;9:618045. doi: 10.3389/fcell.2021.618045. eCollection 2021.
PM. refers to atmospheric particulate matters with a diameter of less than 2.5 μm. The deposit of PM. in lung cells can cause oxidative stress, leading to changes in macrophage polarity, which can subsequently cause pulmonary inflammation. Long-chain non-coding RNA (lncRNA) is a class of transcripts that regulate biological processes through multiple mechanisms. However, the role of lncRNA in PM.-induced lung inflammation has not been established. In this study, the biological effects and associated mechanism of lncRNA in PM.-induced change in macrophage polarity were investigated. The lncRNA-mediated PM.-induced macrophage inflammation and lung inflammation-associated injury were also determined. Mice were exposed to chronic levels of PM., and changes in the expression of lncRNA in the lung were measured by lncRNA microarray. lncRNAs that showed significant changes in expression in response to PM. were identified. lncRNA showing the biggest change was subjected to further analysis to determine its functional roles and mechanisms with respect to macrophage activation. The result showed that a significant reduction in expression of one lncRNA, identified as lncGm16410, was observed in the lung of mice and RAW264.7 cells following exposure to PM.. lncGm16410 suppressed PM.-induced macrophage activation the SRC protein-mediated PI3K/AKT signaling pathway. PM. promoted lung inflammation by downregulating the expression of lncGm16410, enhancing the activation of macrophages. Thus, lncGm16410 might provide new insight into the prevention of PM. injury.
细颗粒物（PM）是指直径小于2.5微米的大气颗粒物。细颗粒物在肺细胞中的沉积可引起氧化应激，导致巨噬细胞极性改变，进而引发肺部炎症。长链非编码RNA（lncRNA）是一类通过多种机制调节生物过程的转录本。然而，lncRNA在细颗粒物诱导的肺部炎症中的作用尚未明确。本研究调查了lncRNA在细颗粒物诱导的巨噬细胞极性变化中的生物学效应及相关机制。还确定了lncRNA介导的细颗粒物诱导的巨噬细胞炎症和肺部炎症相关损伤。将小鼠暴露于慢性水平的细颗粒物中，通过lncRNA微阵列检测肺中lncRNA表达的变化。鉴定出对细颗粒物有显著表达变化的lncRNA。对表达变化最大的lncRNA进行进一步分析，以确定其在巨噬细胞激活方面的功能作用和机制。结果显示，在暴露于细颗粒物后的小鼠肺和RAW264.7细胞中，一种名为lncGm16410的lncRNA表达显著降低。lncGm16410通过SRC蛋白介导的PI3K/AKT信号通路抑制细颗粒物诱导的巨噬细胞激活。细颗粒物通过下调lncGm16410的表达促进肺部炎症，增强巨噬细胞的激活。因此，lncGm16410可能为预防细颗粒物损伤提供新的见解。
