Fig. 1

The proliferation and migration of Dcx-positive cells in a mouse model of neonatal ischemia-reperfusion brain injury. a The timeline of the study design. b Serial coronal T2-weighted MR images at 1 week after brain injury. T2 hyperintensity abnormalities were observed in the cortex and striatum. Five coronal slices were acquired with 1 mm thickness. c Fluorescent image of the ipsilateral (injury) and contralateral (intact) side of SVZ in the model mouse. In the injured SVZ side, the number of Dcx-positive cells began to increase rapidly at 1 week, and was stable thereafter for up to 7 weeks following the injury. Green: Dcx; blue: DAPI. Scale bar = 50 μm. LV lateral ventricle. d Dcx-positive cells were migrated to the injured site at 5 weeks post-injury. Green: Dcx. Scale bar = 200 μm. e In the intact SVZ side, the number of Dcx-positive cells was diminished with advancing age. N = 5 for each time point. The data are presented as the mean numbers of positive cells in the SVZ ± S.D. ^* P < 0.05. f Number of Dcx-positive cells per slice in 1–7 weeks post-injury. Abundant Dcx-positive cells were distributed from the SVZ laterally toward the damaged area. N = 6 for each time point. The data are presented as the mean numbers of positive cells in the ischemic hemisphere (injury side), and the contralateral hemisphere (intact side) ± S.D. ^* P < 0.05, ^** P < 0.01