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. 2016 Feb 15;126(3):1023–1038. doi: 10.1172/JCI84505

Figure 5. VDAC1 silencing and inhibition prevent SC mitochondrial anomalies and improve the phenotype of diabetic mice.

Figure 5

(A) Mitochondrial calcium, (B) cytoplasmic calcium, (C) mitochondrial pH, and (D) motility in mSCs of diabetic mice (db/db) in basal conditions are partially corrected during VDAC1 silencing or blocking. Immunohistochemistry for phospho–c-JUN in mSCs of control and diabetic mice after (E) VDAC1 silencing or (F) TRO19622 treatment. Arrows indicate infected mSC nuclei. Scale bar: 50 μm. Quantification of nuclear phospho–c-JUN represented as fold over control mice (db/+). Noninfected neighbor cells were used as internal controls. (G) Representative transmission electron micrograph images of sciatic nerve cross sections of control (db/+) and diabetic (db/db) mice after vehicle or TRO19622 treatment. Scale bar: 5 μm. (H) Scatterplot showing the g-ratio plotted against the axon diameter of control and diabetic mice treated with vehicle or TRO16922 for 30 days. (I) Average myelin g-ratio, axonal diameter, and number of myelinated axons in sciatic nerves of control and diabetic mice described in H. A minimum of 200 fibers was measured per animal. *P < 0.05, #P < 0.05, **P < 0.01, ##P < 0.01, 1-way ANOVA followed by a Dunnett’s multiple comparison post-hoc test.