In response to ischemic stroke, there is the release of multiple factors that enhance BBB permeability, e.g. ROS, inflammatory mediators and pro-angiogenic factors such as VEGF. Some of the restoration in barrier tightness with time after a stroke is related to reduced levels of those factors, but there is also an upregulation of mediators of barrier quiescence that enhance barrier properties, such as Ang-1. Those mediators can also serve (directly or indirectly) to diminish the effects of the factors enhancing barrier permeability (red lines). Progenitor cells may be directly (integration) or indirectly (mediator release) involved in barrier repair after stroke.