Expression analysis and targets prediction of microRNAs in OGD/R treated astrocyte-derived exosomes by smallRNA sequencing

Astrocytes activate and crosstalk with neurons influencing inflammatory responses following ischemic stroke. The distribution, abundance, and activity of microRNAs in astrocytes-derived exosomes after ischemic stroke remains largely unknown. In this study, exosomes were extracted from primary cultured mouse astrocytes via ultracentrifugation, and exposed to oxygen glucose deprivation/re-oxygenation injury to mimic experimental ischemic stroke. SmallRNAs from astrocyte-derived exosomes were sequenced, and differentially expressed microRNAs were randomly selected and verified by stem-loop real time quantitative polymerase chain reaction. We found that 176 microRNAs, including 148 known and 28 novel microRNAs, were differentially expressed in astrocyte-derived exosomes following oxygen glucose deprivation/re-oxygenation injury. In gene ontology enrichment, Kyoto encyclopedia of genes and genomes pathway analyses, and microRNA target gene prediction analyses, these alteration in microRNAs were associated to a broad spectrum of physiological functions including signaling transduction, neuroprotection and stress responses. Our findings warrant further investigating of these differentially expressed microRNAs in human diseases particularly ischemic stroke.

Automated summary

In this study, exosomes derived from mouse astrocytes were sequenced to investigate the differentially expressed microRNAs following oxygen glucose deprivation/re-oxygenation injury, which mimics ischemic stroke. A total of 176 microRNAs, including known and novel microRNAs, were found to be differentially expressed in astrocyte-derived exosomes. These alterations in microRNAs are associated with a broad range of physiological functions, such as signaling transduction, neuroprotection, and stress responses. Further investigation of these differentially expressed microRNAs in human diseases, especially ischemic stroke, is warranted.