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Expression changes of histone deacetylases in dexamethasone‐induced neurotoxicity in human neuroblastoma SH‐SY5Y cells (LB849)

Chronic stress induces an abnormal increase in glucocorticoids level, which is related with neurodegenerative conditions and mood disorders. Histone deacetylase(HDAC) inhibitors have been suggested to have a promising therapeutic potential for those conditions. However, it is not clear whether HDAC is directly involved in the reverse of glucocorticoid‐mediated stress. We investigated changes of HDAC expression in response to treatment of dexamethasone(Dex), a synthetic glucocorticoid in human neuroblastoma SH‐SY5Y cells. Dex treatment affects cell viability even with 1uM. The stress induction was confirmed with stress‐response genes in neurons such as norepinephrine transporter and monoamine oxidase‐A, which increased in 4.2 and 5.1 folds, respectively. Various HDAC mRNA levels were profiled upon Dex treatment. While expression of HDAC1, 6, and 8 were not changed, HDAC4 and HDAC9 were significantly overexpressed in 1.8 and 2.1 folds, respectively. The direct changes of specific HDACs in reponse to Dex‐induced stress might suggest a potential mechanism by which chronic stress leads to neurodegenerative conditions.