Fig. S3. Protective effect of CB-MSC obtained from 3 different donors on sensory-motor deficit. Sensory-motor deficits were similarly attenuated by CB-MSC obtained from three different cord blood donors (A-CB-MSC, n=16, B-CB-MSC, n=12 or C-CB-MSC, n=12) as assessed by beam walk (A, mean+SD) and neuroscore (B, mean +SD) 7 days after CCI. 1-way ANOVA: Beam walk: p=0.001, neuroscore: p=0.001, post-hoc Tukey’s test **p<0.01, compared to CCI pbs mice.
Fig. S4. Distribution of CB-MSC in sham operated and CCI mice at 7 days after injury. CB-MSC were infused icv contralateral to CCI/sham injury. Microphotographs (D, E) show Hoechst stained cell location in the brain. They appear clustered and confined into the ventricles in sham animals (A-D), while they appear to diffuse in the parenchyma in CCI mice (E-H). Drawings are based on visual observation of 8 brains for each experimental condition, blue dots represent Hoechst stained stem cells.
Fig. S5. Relationship between CB-MSC homing and sensorimotor deficits and anatomical damage. CB-MSC presence into the contused tissue observed 5 weeks after injury did not affect the scores obtained at different time points after injury both at beam walk (A) and composite neuroscore (B) tests. Similarly no differences could be observed in the degree of anatomical damage 5 weeks after CCI. (CB-MSC in contusion, n=5, CB-MSC in ventricles, n=6).
Fig. S6. BDNF production by transplanted CB-MSC and resident cells. Confocal microscopy on CCI CB-MSC mice performed 7 days post-injury revealed that most transplanted Hoechst positive CB-MSC were in close association with BDNF (A-C). In the peri contusional cortex, among resident cells, a close association with BDNF was observed for NeuN positive cells (D-F) and a colabeling with BDNF was observed for most GFAP positive cells (J-L). Conversely no colabeling was detected for CD11b positive cells (G-I) neither for NG-2 (M-O). Bars = 20 µm.