Evidence is mounting that PM2.5 exposure could lead to learning disability, memory deficits, and cognitive impairment; however, the underlying mechanisms are still not well demonstrated yet. Long non-coding RNAs (LncRNAs) play a crucial role in many human diseases. Although the relationship of Alzheimer's disease (AD) and lncRNAs have been discovered, the role of lncRNA in AD-like phenotype induced by PM2.5 needs further exploration. In this study, we profiled the expression of messenger RNAs (mRNAs) and lncRNAs in hippocampus after confirming the AD-like changes in mice. Compared with the control group, a total of 478 mRNAs and 151 lncRNAs were dysregulated after PM2.5 exposure. ECM-receptor interaction, focal adhesion, complement and coagulation cascades, and AGE-RAGE signaling pathway were found dysregulated through lncRNA-co-expressed genes analysis based on the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). Meanwhile, the genes related to microglia were significantly altered, such as CX3CR1, CD163, lncRNA Gm44750, and lncRNA Gm43509. Above evidences suggested that microglia-related lncRNAs dysregulation probably plays a crucial role in PM2.5exposure-associated learning and memory deficits.
Keywords: Alzheimer’s disease; LncRNA; Microglia; Morris water maze test; PM2.5; RNA-seq.
© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.