| First Author | Zhou P | Year | 2014 |
| Journal | PLoS One | Volume | 9 |
| Issue | 5 | Pages | e98275 |
| PubMed ID | 24874187 | Mgi Jnum | J:217342 |
| Mgi Id | MGI:5613773 | Doi | 10.1371/journal.pone.0098275 |
| Citation | Zhou P, et al. (2014) Protection of retina by alphaB crystallin in sodium iodate induced retinal degeneration. PLoS One 9(5):e98275 |
| abstractText | Age-related macular degeneration (AMD) is a leading cause of blindness in the developed world. The retinal pigment epithelium (RPE) is a critical site of pathology in AMD and alphaB crystallin expression is increased in RPE and associated drusen in AMD. The purpose of this study was to investigate the role of alphaB crystallin in sodium iodate (NaIO3)-induced retinal degeneration, a model of AMD in which the primary site of pathology is the RPE. Dose dependent effects of intravenous NaIO3 (20-70 mg/kg) on development of retinal degeneration (fundus photography) and RPE and retinal neuronal loss (histology) were determined in wild type and alphaB crystallin knockout mice. Absence of alphaB crystallin augmented retinal degeneration in low dose (20 mg/kg) NaIO3-treated mice and increased retinal cell apoptosis which was mainly localized to the RPE layer. Generation of reactive oxygen species (ROS) was observed with NaIO3 in mouse and human RPE which increased further after alphaB crystallin knockout or siRNA knockdown, respectively. NaIO3 upregulated AKT phosphorylation and peroxisome proliferator-activator receptor-gamma (PPARgamma) which was suppressed after alphaB crystallin siRNA knockdown. Further, PPARgamma ligand inhibited NaIO3-induced ROS generation. Our data suggest that alphaB crystallin plays a critical role in protection of NaIO3-induced oxidative stress and retinal degeneration in part through upregulation of AKT phosphorylation and PPARgamma expression. |
