Here we report that EPC subtype-specific changes occur in a non-linear fashion in response to developmental programming of increased stroke susceptibility, that fresh cd45- [cd34+/kdr+]EPCs exhibit subset-specific functions and pathway-specific profile changes with age, and that cell-therapy with freshly isolated juvenile cd45- [cd34+/kdr+]EPCs delays the onset of ischemic-hemorrhagic strokes in the spTg25 rat model. This evidence concerns the gene CD34 and hemorrhagic stroke.