| First Author | Dai TL | Year | 2014 |
| Journal | Exp Ther Med | Volume | 8 |
| Issue | 2 | Pages | 384-390 |
| PubMed ID | 25009587 | Mgi Jnum | J:224801 |
| Mgi Id | MGI:5689084 | Doi | 10.3892/etm.2014.1745 |
| Citation | Dai TL, et al. (2014) Depletion of canonical Wnt signaling components has a neuroprotective effect on midbrain dopaminergic neurons in an MPTP-induced mouse model of Parkinson's disease. Exp Ther Med 8(2):384-390 |
| abstractText | The canonical Wnt signaling pathway is critical for the development of midbrain dopaminergic (DA) neurons, and recent studies have suggested that disruption of this signaling cascade may underlie the pathogenesis of Parkinson's disease (PD). However, the exact role of the canonical Wnt signaling pathway, including low-density lipoprotein receptor-related protein 5 and 6 (LRP5/6) and beta-catenin components, in a mouse model of PD remains unclear. In the present study, the tyrosine hydroxylase (TH)-Cre transgenic mouse line was used to generate mice with the specific knockout of LRP5, LRP6 or beta-catenin in DA neurons. Following inactivation of LRP5, LRP6 or beta-catenin, TH-immunohistochemical staining was performed. The results indicated that beta-catenin is required for the development or maintenance of these neurons; however, LRP5 and LRP6 were found to be dispensable. In 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice, the depletion of LRP5, LRP6 or beta-catenin was found to be protective for the midbrain DA neurons to a certain extent. These in vivo results provide a novel perspective for the function of the canonical Wnt signaling pathway in a mouse model of PD. |
