Fig. 6: S1P/PPARg dependent regulation of lipid metabolism and SC reprogramming in mice.

a, b qPCR analysis of genes involved in lipid metabolism in control or injured murine nerves treated with 4-deoxypyridoxine (DOP; a) or pioglitazone (PIO; b). Expression at 0 h was set to one and the fold change was calculated for the other time points. Biological replicates analysed: n = 9 and n = 4 for each condition for (a) and (b) respectively. c–h qPCR analysis of the marker genes for repair SCs Shh and Gdnf and the myelin gene Mbp in control or injured murine nerves treated with DOP (c–e) or PIO (f–h). Expression at 0 h was set to one and the fold change was calculated for the other time points. Biological replicates analysed: n = 9 for c–e and n = 4 for f–h for each condition. i–k Histological analysis of cJUN protein expression (i), MBP (j) and βIII tubulin⁺ axons (k) in murine nerves without injury (0 h) or 48 h after injury with control (w/o PIO) or with pioglitazone (+ PIO) treatment. Scale is 25 µm. l Quantification of cJUN⁺ cells per nerve area. Biological replicates: n = 9, 7 and 4 for 0 h, 48 h and 48 h + PIO. m Quantification of MBP⁺ area per nerve area. Biological replicates: n = 7, 7 and 4 for 0 h, 48 h and 48 h + PIO. n Quantification of the relative βIIITUB⁺ area per nerve area. Time point 0 h was set to 100%. Biological replicates: n = 7, 7 and 4 for 0 h, 48 h and 48 h + PIO. Each dot represents a single mouse nerve. 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–h, l–m are provided as a Source Data file.