| First Author | Wang P | Year | 2017 |
| Journal | Oxid Med Cell Longev | Volume | 2017 |
| Pages | 1020357 | PubMed ID | 28191272 |
| Mgi Jnum | J:332141 | Mgi Id | MGI:7408629 |
| Doi | 10.1155/2017/1020357 | Citation | Wang P, et al. (2017) Mitochondrial Ferritin Deletion Exacerbates beta-Amyloid-Induced Neurotoxicity in Mice. Oxid Med Cell Longev 2017:1020357 |
| abstractText | Mitochondrial ferritin (FtMt) is a mitochondrial iron storage protein which protects mitochondria from iron-induced oxidative damage. Our previous studies indicate that FtMt attenuates beta-amyloid- and 6-hydroxydopamine-induced neurotoxicity in SH-SY5Y cells. To explore the protective effects of FtMt on beta-amyloid-induced memory impairment and neuronal apoptosis and the mechanisms involved, 10-month-old wild-type and Ftmt knockout mice were infused intracerebroventricularly (ICV) with Abeta(25-35) to establish an Alzheimer's disease model. Knockout of Ftmt significantly exacerbated Abeta(25-35)-induced learning and memory impairment. The Bcl-2/Bax ratio in mouse hippocampi was decreased and the levels of cleaved caspase-3 and PARP were increased. The number of neuronal cells undergoing apoptosis in the hippocampus was also increased in Ftmt knockout mice. In addition, the levels of L-ferritin and FPN1 in the hippocampus were raised, and the expression of TfR1 was decreased. Increased MDA levels were also detected in Ftmt knockout mice treated with Abeta(25-35). In conclusion, this study demonstrated that the neurological impairment induced by Abeta(25-35) was exacerbated in Ftmt knockout mice and that this may relate to increased levels of oxidative stress. |
