RNA-seq analysis of differentiated noradrenergic neurons (1C11NE) and microglia (BV2) following exposure to acrylamide (ACR)

Neurotoxicity of acrylamide (ACR), which is an environmental electrophilic chemical, has been reported in occupational human cases and experimental animal models. Our previous study using murine model demonstrated that exposure to ACR induced dose-dependent degeneration of noradrenergic axons, which has been reported to be extensively related with various cognitive disorders and neurodegenerative diseases. To investigate the mechanism of ACR-induced degeneration of noradrenergic neurons and the role of microglia, in this study, differentiated noradrenergic neuron model (1C11NE), as well as microglia cell line (BV2) were used. BV2 microglia were exposed to PBS or ACR (1mM) for 24 hrs. 1C11NE neurons were exposed to ACR or to conditioned medium (CM) from ACR-treated BV2 microglial cells (ACR-CM). Transcriptomic RNA-seq were carried out for 1C11NE neurons and BV2 microglia.