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. Overall design: For 1C11NE neurons, five groups of samples after different treatments for 24 hrs were analyzed, including: 1) PBS group, 1C11NE cells were exposed to vehicle PBS, (i.e. 0 mM ACR); 2) ACR group, 1C11NE cells were exposed to 1mM ACR; 3) PBS-CM group, 1C11NE cells were exposed to CM of PBS-exposed BV2 microglia; 4) ACR-CM group, 1C11NE cells were exposed to CM of 1mM ACR-exposed BV2 microglia; 5) PBS-CM+ACR group, 1C11NE cells were exposed to PBS-CM with addition of 1mM ACR. For BV2 microglia, two groups of samples were analyzed, including: 1) BV2_PBS group, BV2 cells were exposed to vehicle PBS, (i.e. 0 mM ACR); 2) BV2_ACR group, BV2 cells were exposed to 1mM ACR.