| First Author | Liu Y | Year | 2014 |
| Journal | Brain Res | Volume | 1588 |
| Pages | 17-24 | PubMed ID | 25223908 |
| Mgi Jnum | J:217899 | Mgi Id | MGI:5616033 |
| Doi | 10.1016/j.brainres.2014.09.018 | Citation | Liu Y, et al. (2014) Deficiency of Trim27 protects dopaminergic neurons from apoptosis in the neurotoxin model of Parkinson's disease. Brain Res 1588:17-24 |
| abstractText | Parkinson's disease (PD) is an age-related neurodegenerative movement disorder, characterized by loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). The MPTP/MPP+ model is often used to investigate the signaling mechanisms of dopamine (DA) degeneration, both in vivo and in vitro. The identification of specific genetic and environmental factors responsible for PD has bolstered evidence for a shared pathway of neuronal death -apoptosis. Trim27 is reported to promote apoptosis. However, little evidence exists to indicate a linkage between Trim27 and PD. In this study, we found that compared to healthy individuals, Trim27 was significantly upregulated in patients with PD. We further showed that Trim27 expression was dramatically induced in PC12 cells and in the SNpc of the PD mouse model. RNAi-mediated knockdown of Trim27 in PC12 cells showed obvious suppression of apoptosis. There are reduced dopaminergic neuron loss and lower apoptotic protein expression levels in MPTP-treated Trim27-/- mice, compared with MPTP-treated WT mice. These data demonstrated that Trim27 deficiency decreases apoptosis and protects dopaminergic neurons in the neurotoxin model of PD, suggesting that Trim27 may be an effective potential target during the treatment of PD. |
