| First Author | Xie N | Year | 2014 |
| Journal | Neuroscience | Volume | 256 |
| Pages | 36-42 | PubMed ID | 24144623 |
| Mgi Jnum | J:207637 | Mgi Id | MGI:5559271 |
| Doi | 10.1016/j.neuroscience.2013.10.011 | Citation | Xie N, et al. (2014) Inhibition of mitochondrial fission attenuates Abeta-induced microglia apoptosis. Neuroscience 256:36-42 |
| abstractText | Mitochondrial division inhibitor 1 (mdivi-1), a selective inhibitor of mitochondrial fission protein dynamin-related protein 1 (Drp1), has been reported to display neuroprotective properties in different animal models. In the present study, we investigated the protective effect of mdivi-1 on beta-amyloid protein (Abeta)-induced cytotoxicity and its potential mechanisms in BV-2 and primary microglial cells. We found that mitochondrial fission was increased in Abeta treatment and inhibition of mitochondrial fission by mdivi-1 significantly reduced Abeta-induced expression of CD11b (a marker of microglial activation), viability loss and apoptotic rate increase in BV-2 and primary microglial cells. Moreover, we also found that mdivi-1 treatment markedly reversed mitochondrial membrane potential loss, cytochrome c (CytC) release and caspase-3 activation. Altogether, our data suggested that mdivi-1 exerts neuroprotective effects against Abeta-induced microglial apoptosis, and the underlying mechanism may be through inhibiting mitochondrial membrane potential loss, CytC release and suppression of the mitochondrial apoptosis pathway. |
