First Author | Chen B | Year | 2019 |
Journal | Invest Ophthalmol Vis Sci | Volume | 60 |
Issue | 4 | Pages | 1165-1174 |
PubMed ID | 30908580 | Mgi Jnum | J:273695 |
Mgi Id | MGI:6285444 | Doi | 10.1167/iovs.18-25751 |
Citation | Chen B, et al. (2019) A Mouse Model of Retinal Recovery From Photo-Oxidative/Photo-Inflammatory Injury: Nrf2, SOD1, DJ-1, and Parkin Are Not Essential to Recovery. Invest Ophthalmol Vis Sci 60(4):1165-1174 |
abstractText | Purpose: To determine if there is structural and functional recovery of the retina from light induced retinal degeneration, and to evaluate the role of the oxidative stress response elements Nrf2, SOD1, DJ-1, and Parkin in such a recovery process. Methods: Eyes from C57BL/6J (B6J) mice and from oxidative stress response-deficient strains of mice were treated with intense light using the fundus camera-delivered light-induced retinal degeneration (FCD-LIRD) model. Fundus photographs, optical coherence tomography (OCT) images, and electroretinography (ERG) responses were obtained before the injury, during the "maximal injury phase" (days 4-7) and during the "recovery phase" (days 14-16) post light exposure and were evaluated for retinal damage and assessed for evidence of recovery from the injury. Results: We demonstrate that mice treated with a sub-lethal FCD-LIRD protocol show an initial acute retina injury phase peaking between days 4 to 7 followed by a recovery phase in which the outer retinal thickness/volume and retinal function partially recover. These observations are reproduced in B6J mice and in mice lacking oxidative stress response enzymes (SOD1, DJ-1, and Parkin) or the oxidative stress response master regulator Nrf2. Conclusions: Our data indicate that retinal recovery from injury can proceed via pathways that are independent from the common oxidative stress response elements Nrf2, SOD1, DJ-1, and Parkin. Furthermore, the model of retinal recovery from injury that we describe here mimics changes seen in a variety of clinical entities and may provide an excellent platform for dissecting general pathways of retinal recovery from sub-lethal injury. |