Figure 2: Tcf7l2 ablation impairs remyelination in LPC-induced demyelinating animal model.

(a,b) Expression of Mbp in the spinal cord from control (Ctrl) and Tcf7l2ΔHMG mice at indicated neonatal and adult ages by in situ hybridization. (c) Electron microscopy of the spinal white matter of control and Tcf7l2ΔHMG mice at P60. The percentages of myelinated axons (d) and g-ratio (e) in the spinal white matter of control and Tcf7l2ΔHMG mice at P60. The data represent the means±s.e.m.; n=3 animals per genotype. (f) Left: the location of LPC-induced lesion (DAPI counterstaining, dashed lines) in the spinal cord. Right: in situ hybridization analysis showed re-expression of Tcf7l2 in the LPC-induced demyelinating lesions (demarcated with dashed lines) and uninjured regions at 7 and 14 dpl in spinal cords of P60 mice. (g) In situ hybridization analysis of PDGFRα, Mbp and Plp1 in the lesion regions (demarcated with dashed lines) at 14 dpl in spinal cords of P60 Ctrl and Tcf7l2ΔHMG mutant mice. Quantification of the numbers of PDGFRα⁺ OPC (h) and Plp1⁺ OL (i) at 14 dpl in spinal cords of P60 control and Tcf7l2ΔHMG mutant mice; n=5 animals for each genotype. (j) Representative electron micrographs of spinal cords of 8-week-old control and Tcf7l2ΔHMG mice at 14 dpl. Arrow indicates the newly formed thin myelin sheath. (k) Quantification of the percentage newly myelinated axons in spinal lesions of 8-week-old control and Tcf7l2ΔHMG mice at 14 dpl; n=3 animals for each genotype. (l) Quantification of g-ratio of newly myelinated axons in spinal lesions of 8-week-old control and Tcf7l2ΔHMG mice at 14 dpl; n=3 animals for each genotype. P<0.001, Student’s t-test. Data are presented as mean±s.e.m. **P<0.01, ***P<0.001; Student’s t-test. Scale bars, 100 μm (a,b), 2 μm (c,j) and 50 μm (f,g).