神经药理学报 ›› 2017, Vol. 7 ›› Issue (2): 57-57.
YANG Cui-cui，KUAI Xue-xian，LI Ya-li，ZHANG Li，LI Lin，ZHANG Lan
摘要： PP2Ac demethylation is regulated by LCMT （a specific leucine carboxyl methyltransferase catalyzing methylation of PP2A） and PME （a specific methylesterase catalyzing demethylation of PP2A. Objective：The aim of the present study was to investigate the mechanism of Cornel iridoid glycoside （CIG） on PP2A catalytic subunit C （PP2Ac）. Methods：We used recombined lentivirus vector to deliver PME-1 genetic materials into N2a cells or transfected LCMT-1 siRNA into N2a cells to block the expression of LCMT-1. Twenty-four hours later，cells were rinsed twice with cold PBS （pH 7.4） and CIG at different concentrations （50，100，and 200 μg·mL-1，respectively） were added for 24 h. Western blotting was used to PP2Ac、demethylaion/methylation PP2Ac、LCMT-1 and PME-1. The activity of PP2A was detected by a biochemical assay. Results：①Lentivirus transferred PME- 1 was expressed at high level in the N2a cells after transduction. Correspondingly，the demethylation of PP2Ac was increasing and PP2A activity was decreasing after transduction. Treatment with CIG for 24 h reversed the increase of PME-1 and demethylation of PP2Ac without influencing LCMT-1 expression. PP2A activity was also signifi cantly enhanced in CIG treatment group，compared with the cells after PME-1 transduction. ②LCMT-1 siRNA signifi cantly decreased LCMT-1 expression. CIG did not affect LCMT-1expression. however，demethylation of PP2Ac is increased in siRNA-transfected cells and CIG could reversed the high demethylation of PP2Ac and PP2A activity. Conclusion：CIG increases methylation of PP2A subunit C by inhibiting PME-1.
