| First Author | Xu L | Year | 2020 |
| Journal | Redox Biol | Volume | 37 |
| Pages | 101700 | PubMed ID | 32863184 |
| Mgi Jnum | J:329682 | Mgi Id | MGI:6802394 |
| Doi | 10.1016/j.redox.2020.101700 | Citation | Xu L, et al. (2020) Retinal homeostasis and metformin-induced protection are not affected by retina-specific Ppardelta knockout. Redox Biol 37:101700 |
| abstractText | Peroxisome proliferator-activated receptors (PPARs) are a family of three nuclear hormone receptors (PPARalpha, PPARdelta, and PPARgamma) that are known to regulate expression of lipid metabolism and oxidative stress genes. Given their role in reducing oxidative stress in a variety of tissues, these genes are likely important for retinal homeostasis. This hypothesis has been further supported by recent studies suggesting that PPAR-activating drugs are protective against retinal degenerations. The objective of the present study was to determine the role of PPARdelta in the neuroretina. RNA-seq data show that Pparalpha and Ppardelta are both expressed in the retina, but that Ppardelta is expressed at 4-fold higher levels. Single-cell RNAseq data show that Ppardelta is broadly expressed in all retinal cell types. To determine the importance of Ppardelta to the retina, we generated retina-specific Ppardelta knockout mice. We found that deletion of Ppardelta had a minimal effect on retinal function or morphology out to 12 months of age and did not increase retinal sensitivity to oxidative stress induced by exposure to bright light. While data show that PPARdelta levels were increased by the drug metformin, PPARdelta was not necessary for metformin-induced protection from light damage. These data suggest that Ppardelta either has a redundant function with Pparalpha or is not essential for normal neuroretina function or resistance to oxidative stress. |
