Fig. 3: Mitochondrial functional and morphological anomalies are present in the muscles of Icos-/- NOD mice.
From: IFNγ causes mitochondrial dysfunction and oxidative stress in myositis
a Histoenzymology COX, NADH-TR, and SDH stainings of Icos-/- NOD and Icos+/+ NOD mice muscles at 8, 25, and 35 weeks of age (predisease, onset, and established disease stages) (representative images from n = 10 independent mice/genotype and age analyzed). For Icos-/- NOD mice at 35 weeks of age, two lower and two higher magnification representative images are shown. Arrows point at pale myofibers or dark fibers exhibiting loss of staining areas. Scale bars, 100 µm. Quantification of COXhigh fibers on images of entire quadriceps sections is shown on the right graph (n = 5 independent mice/genotype/age except for Icos-/- NOD mice at 35 weeks of age, with n = 8 independent mice). Statistical analysis was performed using the Two-way ANOVA test with Sidak’s post-hoc multicomparison. b Ex vivo analysis of oxygen consumption (respiratory control ratio) in Icos-/- NOD (n = 4 independent mice) and Icos+/+ NOD mice (n = 5 independent mice) skinned muscles fibers. Statistical analyses were performed using the Mann–Whitney test (two-tailed). Mean values ± s.e.m are shown. c Electron microscopy representative images of muscles from Icos-/- NOD and Icos+/+ NOD mice. a–c were repeated independently twice. Numbers on panels denote p values. Source data are provided as a Source Data file.
