| First Author | Hass DT | Year | 2019 |
| Journal | Front Neurosci | Volume | 13 |
| Pages | 201 | PubMed ID | 30906248 |
| Mgi Jnum | J:281068 | Mgi Id | MGI:6376433 |
| Doi | 10.3389/fnins.2019.00201 | Citation | Hass DT, et al. (2019) Cell Autonomous Neuroprotection by the Mitochondrial Uncoupling Protein 2 in a Mouse Model of Glaucoma. Front Neurosci 13:201 |
| abstractText | Glaucoma is a group of disorders associated with retinal ganglion cell (RGC) degeneration and death. There is a clear contribution of mitochondrial dysfunction and oxidative stress toward glaucomatous RGC death. Mitochondrial uncoupling protein 2 (Ucp2) is a well-known regulator of oxidative stress that increases cell survival in acute models of oxidative damage. The impact of Ucp2 on cell survival during sub-acute and chronic neurodegenerative conditions, however, is not yet clear. Herein, we test the hypothesis that increased Ucp2 expression will improve RGC survival in a mouse model of glaucoma. We show that increasing RGC but not glial Ucp2 expression in transgenic animals decreases glaucomatous RGC death, but also that the PPAR-gamma agonist rosiglitazone (RSG), an endogenous transcriptional activator of Ucp2, does not significantly alter RGC loss during glaucoma. Together, these data support a model whereby increased Ucp2 expression mediates neuroprotection during a long-term oxidative stressor, but that transcriptional activation alone is insufficient to elicit a neuroprotective effect, motivating further research in to the post-transcriptional regulation of Ucp2. |
