Fig. 1

Essential role of PPARα in retinal neuronal survival. a Longitudinal electroretinography revealed that retinal function (rod and cone A-waves and B-waves) declined in Pparα ^-/- mice relative to wild-type (WT) starting at 7 weeks (7, 9, 11, and 26 weeks, n = 5 mice/genotype; 52 weeks, n = 8 mice/genotype). b Cross-sectional optical coherence tomography demonstrated that total retinal thickness progressively declined in Pparα ^-/- mice and remained constant in WT (13 weeks, n = 9 mice/genotype; 26 weeks, WT n = 9, Pparα ^-/- n = 8; 60 weeks, n = 8 mice/genotype). c Retinal cell death ELISA identified that total retinal apoptosis was significantly increased in Pparα ^-/- retinas relative to WT beginning at 8 weeks of age (n = 5 retinas/genotype per time point). d Retinal GFAP levels were increased in Pparα ^-/- retinas relative to WT, suggesting retinal gliosis (8, 15 weeks, n = 5 retinas/genotype; 40 weeks, n = 6 retinas/genotype). e Retinal cell death ELISA revealed that total retinal apoptosis was significantly increased in Vdllr ^-/- mice and restored to baseline by treatment with PPARα agonist fenofibric acid (Feno) (WT Veh, n = 7; WT Feno, n = 8; Vdllr ^-/- Veh, n = 7; Vdllr ^-/- Feno, n = 8). Data are expressed as mean ± SEM. *P ≤ 0.05; **P ≤ 0.01; ***P ≤ 0.001; ****P ≤ 0.0001, unpaired two-tailed Student’s t test (a–d) or one-way ANOVA with Tukey’s post-hoc comparison (e)