Figure 6: Targeted overexpression of ADFm specifically within endothelial cells improves long-term neurological functions after cerebral ischaemic injury in vivo.

(a–d) Neurobehavioral tests were performed on WT and EC-specific ADFm-overexpressing mice before and 1–28 d after tFCI or sham operation. Sensorimotor deficits were evaluated by the rotarod test (a), cylinder test (b) and corner test (c). L, left; R, right; B, both forepaws in b. (d) Long-term cognitive deficits were assessed in the Morris water maze at 23–28 d after tFCI. The time needed for the animal to locate the submerged platform (escape latency) was measured from 23 to 27 d after tFCI. Spatial memory was evaluated at 28 d after tFCI by measuring the time spent in the target quadrant when the platform was removed. Gross locomotor functions, as reflected by similar swim speeds, were not affected by transgene expression. (e) Brain atrophy at 28 d after tFCI was quantified on MAP2 (green)-stained coronal sections. Dashed lines outline the relative area of the uninjured contralateral hemisphere to illustrate by comparison the area of ipsilateral atrophy. Scale bar, 1 mm. n=8–9 mice per group. *P≤0.05, **P≤0.01 versus WT. d, days.