| First Author | Park HJ | Year | 2014 |
| Journal | Neurobiol Aging | Volume | 35 |
| Issue | 8 | Pages | 1920-8 |
| PubMed ID | 24629674 | Mgi Jnum | J:214864 |
| Mgi Id | MGI:5604090 | Doi | 10.1016/j.neurobiolaging.2014.01.028 |
| Citation | Park HJ, et al. (2014) Neuroprotective effects of mesenchymal stem cells through autophagy modulation in a parkinsonian model. Neurobiol Aging 35(8):1920-8 |
| abstractText | Autophagy is a major degradation pathway for abnormal aggregated proteins and organelles that cause various neurodegenerative diseases. Current evidence suggests a central role for autophagy in pathogenesis of Parkinson's disease, and that dysfunction in the autophagic system may lead to alpha-synuclein accumulation. In the present study, we investigated whether mesenchymal stem cells (MSCs) would enhance autophagy and thus exert a neuroprotective effect through the modulation of alpha-synuclein in parkinsonian models. In MPP(+)-treated neuronal cells, coculture with MSCs increased cellular viability, attenuated expression of alpha-synuclein, and enhanced the number of LC3-II-positive autophagosomes compared with cells treated with MPP(+) only. In an MPTP-treated animal model of Parkinson's disease, MSC administration significantly increased final maturation of late autophagic vacuoles, fusion with lysosomes. Moreover, MSC administration significantly reduced the level of alpha-synuclein in dopaminergic neurons, which was elevated in MPTP-treated mice. These results suggest that MSC treatment significantly enhances autophagolysosome formation and may modulate alpha-synuclein expression in parkinsonian models, which may lead to increased neuronal survival in the presence of neurotoxins. |
