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Stress is ever present in our modern, performance-oriented and demanding society, which causes adverse stress reactions of the body and affects health seriously. Chronic stress has been recognized as a significant risk factor leading to cognitive impairment, but the underlying mechanism is far from fully understood. Norepinephrine (NE), a pivotal stress-induced hormone, has been found to induce cell apoptosis. However, the function and the key downstream mediator of NE on the regulation of hippocampal neurons still need further exploration. In this study, we explored the role of NE in neuronal apoptosis and its association with MALAT1. Flow cytometry assay and automated western bot assay were carried out to evaluate the cell apoptosis. The data showed that the rate of apoptosis rate and the levels of apoptotic proteins (cleaved-Caspase3 and cleaved-PARP) were significantly increased in HT22 cells after a high dose of NE treatment, suggesting a facilitative role of NE on hippocampal neuronal apoptosis. Besides, a high level of NE up-regulated the expression of MALAT1 in HT22 cells. Then, a lentivirus expressing MALAT1 shRNA was constructed to investigate the role of MALAT1 in cell apoptosis and the results revealed that MALAT1 depletion decreased the cell apoptosis. Moreover, the knockdown of MALAT1 abolished the discrepancy in apoptosis between NE-treated cells and control cells. In conclusion, a high level of the stress-induced hormone NE promoted apoptosis of hippocampal neurons by elevating the expression of MALAT1. Our findings provide new experimental data supporting the epigenetic mechanisms in the regulation of stress response and may provide a potential therapeutic target for stress-related cognition dysfunction.

Norepinephrine promotes neuronal apoptosis of hippocampal HT22 cells by up-regulating the expression of long non-coding RNA MALAT1