摘要
To investigate the molecular mechanism underlying the neuroprotective effect of lithium on cells, in this study, we exposed SH-SY5Y cells to 0.5 mmol/L lithium carbonate （Li2CO2） for 25-50 weeks and then detected the expression levels of some neurobiology related genes and post-translational modifications of stress proteins in SH-SYSY cells, cDNA arrays showed that pyruvate kinase 2 （PKM2） and calmodulin 3 （CaM 3） expression levels were significantly down-regulated, phosphatase protein PP2A expression was lightly down-regulated, and casein kinase II （CK2）, threonine/tyrosine phosphatase 7 （PYST2）, and dopamine beta-hydroxylase （DBH） expression levels were significantly up-regulated. Besides, western blot analysis of stress proteins （HSP27, HSP70, GRP78 and GRP94） showed an over-expression of two proteins： a 105 kDa protein which is a hyper-phosphorylated isoform of GRP94, and a 108 kDa protein which is a phosphorylated tetramer of HSP27. These results suggest that the neuroprotective effects of lithium are likely related to gene expressions and post-translational modifications of proteins cited above.
To investigate the molecular mechanism underlying the neuroprotective effect of lithium on cells, in this study, we exposed SH-SY5Y cells to 0.5 mmol/L lithium carbonate （Li2CO2） for 25-50 weeks and then detected the expression levels of some neurobiology related genes and post-translational modifications of stress proteins in SH-SYSY cells, cDNA arrays showed that pyruvate kinase 2 （PKM2） and calmodulin 3 （CaM 3） expression levels were significantly down-regulated, phosphatase protein PP2A expression was lightly down-regulated, and casein kinase II （CK2）, threonine/tyrosine phosphatase 7 （PYST2）, and dopamine beta-hydroxylase （DBH） expression levels were significantly up-regulated. Besides, western blot analysis of stress proteins （HSP27, HSP70, GRP78 and GRP94） showed an over-expression of two proteins： a 105 kDa protein which is a hyper-phosphorylated isoform of GRP94, and a 108 kDa protein which is a phosphorylated tetramer of HSP27. These results suggest that the neuroprotective effects of lithium are likely related to gene expressions and post-translational modifications of proteins cited above.
