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. 2017 Nov 28;15:113. doi: 10.1186/s12915-017-0451-x

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© Ma et al. 2017

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 5 — Diminished mitochondrial function in Pparα ^-/- retinas. a–d Basal and maximal mitochondrial oxygen consumption rate (OCR) were decreased in (a, b) 8-week-old and (c, d) 12-week-old Pparα ^-/- retinas relative to age-matched wild-type (WT) controls (WT 8 weeks, n = 17; Pparα ^-/- 8 weeks, n = 20; WT 12 weeks, n = 21; Pparα ^-/- 12 weeks, n = 15). e Retinal NADH oxidation was decreased in Pparα ^-/- retinas relative to age-matched WT controls beginning at 8 weeks of age (8 weeks WT, n = 10; Pparα ^-/-, n = 9; 18 weeks, n = 6/genotype; 60 weeks, n = 3/genotype). f Retinal NADH oxidation was decreased in 11-week-old Vldlr ^-/- retinas and restored by treatment with PPARα agonist fenofibric acid (Feno) (WT Veh, n = 7; WT Feno-FA, n = 8; Vdllr ^-/- Veh, n = 7; Vdllr ^-/- Feno-FA, n = 8). g Transmission electron microscopy revealed that at 40 weeks of age, photoreceptor mitochondria had an “active” compressed morphology in WT retinas, and an “inactive” orthodox morphology in Pparα ^-/- retinas (n = 3/genotype). *P ≤ 0.05; **P ≤ 0.01; ***P ≤ 0.001; ****P ≤ 0.0001, unpaired two-tailed Student’s t test (a–e) or one-way ANOVA with Tukey’s post-hoc comparison (f)