TET2 在帕金森病细胞模型中的表达及机制研究.

Objective: Currently, the illlderlying mechanisms of Parkinson's disease (PD) still remain unknown. This study mainly investigated the novel epigenetic markcrs and explored the pathogenesis of PD in the cellular model. Methods: The neuroblastoma cell line SH-SY5Y were used in this study. Fristly, we used CCK-8 to detect cell viability and select the optimal concentration of MPP+ for SH-SY5Y cells. Next, SH-SY5Y cells wcre treated with PBS and MPP+ respectively, then the mRNA e xpression levels of several methylases and demethylases, such as DNMTl, DNMT3A, DNMT3B, TETl, TET2 and TET3 were detected by RT-q PCR, and level ofTET2 protein was detected b y western blot. Finally, the protein localization ofTET2 was detected by immilllofluorescence. Furthermore, we knockdown TET2 with a lentivirus to detect cell proliferation. Results: With the increase of time period orconcentration, the cell inhibition rates increased, we finally select a concentration at which the cell inhibition rate was about 50 %, which turned out to be 2.5 mM. We observed that TET2 was significantly up-regulated and recruited to the nuclear bodies of SH-SY5Y cells after MPP+ treatment. And the CCK-8 assays showed that MPP+ inhibited the proliferation of SH-SY5Y cell lines, while down-regulation ofTET2 promoted proliferation. Conclusions: In the present study, we reporte d the functions of TET2 proteins in the pathogenesis of PD as novel epigenetic markcrs, suggesting that we could use TET2 inhibitors to treat PD in the future, so this study may provide us a new direction and target for PD treatment. [ABSTRACT FROM AUTHOR]