Abstract：
As a dominating air pollutant, atmospheric fine particulate matter within 2.5 μm in diameter (PM2.5) has attracted increasing attention from the researchers all over the world, which will lead to various adverse effects on the central nervous system (CNS), yet the potential mechanism is unclear. In this study, the microglia (BV2 cell line) were exposed to different concentrations of PM2.5 (5, 10 and 20 μg/cm2) for 24 h. It was found that PM2.5 could result in adverse effects on microglia such as decreased cell viability, structural damage and even cell death. And it was reported that long non-coding RNAs (lncRNAs) could participate in multitudinous neurological diseases. Therefore, the microarray analysis was conducted in order to disclose the underlying neurotoxicity mechanism of PM2.5 by ascertaining the differentially expressed lncRNAs (DElncRNAs). The consequences indicated that the DElncRNAs were enriched in various biological pathways, including ferroptosis, IL-17 signaling pathway and NOD-like receptor signaling pathway. Moreover, the cis- and trans-regulated mRNAs by DElncRNAs as well as the corresponding transcriptional factors (TFs) were observed, such as CEBPA, MYC, MEIS1 and KLF4. In summary, our study supplies some candidate libraries and potential preventive target against PM2.5-induced toxicity through targeting lncRNAs. Furthermore, the post-transcriptional regulation will contribute to the future research on PM2.5-induced neurotoxicity.
摘要：
作为主要的空气污染物，直径在2.5μm以内的大气细颗粒物(PM2.5)日益受到世界各国研究者的关注,这将导致对中枢神经系统（CNS）的各种不利影响，然而潜在的机制尚不清楚.在这项研究中,将小胶质细胞（BV2细胞系）暴露于不同浓度的PM2.5（5、10和20μg/cm2）24小时。发现PM2.5会对小胶质细胞产生不利影响，例如细胞活力降低，结构损伤甚至细胞死亡。据报道，长链非编码RNA（lncRNAs）可能参与多种神经系统疾病。因此,进行微阵列分析是为了通过确定差异表达的lncRNAs（DElncRNAs）来揭示PM2.5的潜在神经毒性机制。结果表明，DElncRNAs在各种生物途径中富集，包括铁性凋亡,IL-17信号通路和NOD样受体信号通路。此外，观察到DElncRNAs的顺式和反式调节的mRNA以及相应的转录因子（TFs），如CEBPA,MYC,MEIS1和KLF4。总之,我们的研究通过靶向lncRNAs提供了一些候选文库和针对PM2.5诱导毒性的潜在预防靶点.此外，转录后调控将有助于未来对PM2.5诱导的神经毒性的研究。
