| First Author | Peng Q | Year | 2022 |
| Journal | Front Mol Neurosci | Volume | 15 |
| Pages | 1046992 | PubMed ID | 36479526 |
| Mgi Jnum | J:331993 | Mgi Id | MGI:7407575 |
| Doi | 10.3389/fnmol.2022.1046992 | Citation | Peng Q, et al. (2022) Galectin-9/Tim-3 pathway mediates dopaminergic neurodegeneration in MPTP-induced mouse model of Parkinson's disease. Front Mol Neurosci 15:1046992 |
| abstractText | Galectin-9 (Gal-9) is a crucial immunoregulatory mediator in the central nervous system. Microglial activation and neuroinflammation play a key role in the degeneration of dopaminergic neurons in the substantia nigra (SN) in Parkinson's disease (PD). However, it remains unknown whether Gal-9 is involved in the pathogenesis of PD. We found that MPP(+) treatment promoted the expression of Gal-9 and pro-inflammatory cytokines (IL-6, IL-1beta, TNF-alpha, and MIP-1alpha) in a concentration-dependent manner in BV2 cells. Gal-9 enhanced neurodegeneration and oxidative stress induced by MPP(+) in SH-SY5Y cells and primary neurons. Importantly, deletion of Gal-9 or blockade of Tim-3 ameliorated microglial activation, reduced dopaminergic neuronal loss, and improved motor performance in an MPTP-induced mouse model of PD. These observations demonstrate a pathogenic role of the Gal-9/Tim-3 pathway in exacerbating microglial activation, neuroinflammation, oxidative stress, and dopaminergic neurodegeneration in the pathogenesis of PD. |
