Fig. 7: Human SCs are responsive to pharmacological PPARg modulation.

a qPCR analysis of genes involved in lipid metabolism in control or injured human nerves treated with pioglitazone (PIO). Expression at 0 h was set to one and the fold change was calculated for the other time points. Numbers in bars indicate independent samples analysed. P value for 48 h vs. 48 h + PIO = 0.0043 each for Pparg, Acaca, Fasn and Dgat2. b–d Histological analysis of cJUN protein expression (b), MBP⁺ area (c) and βIIITUB⁺ axons (d) in human nerves without injury (0 h) or 48 h after injury with control (w/o PIO) or with pioglitazone (+ PIO) treatment. Scale: 25 µm. e–g Quantification of cJUN⁺ cells per nerve area (e), MBP⁺ area per nerve area (f) and relative βIIITUB⁺ area per nerve area (g). Time point 0 h was set to 100% for (g). h qPCR analysis of genes involved in lipid metabolism in control or injured human nerves treated with the PPARg antagonists SR16832 (SR) and GW9662 (GW). Expression at 0 h was set to one and the fold change was calculated for the other time points. Numbers in bars indicate independent samples analysed (n.a., not available). Each dot or circle represents a single human nerve analysed. Biological replicates analysed: for a n = 6, 6 and 5 for 0 h, 48 h and 48 h + PIO respectively, for e–g n = 3 for each condition, for h n = 6, 6, 3 and 3, 0 h, 48 h, 48 h + GW and 48 h + SR respectively. Bars in all graphs show mean with SD. Two-sided Mann–Whitney test was used to calculate statistical significance (*P < 0.05, **P < 0.005, ***P < 0.001). Source data for a, e–h are provided as a Source Data file.