Roles of urokinase plasminogen activator receptor expressed in endothelial cells on deterioration of ischemic stroke

在本研究中，我们观察到uPAR基因缺陷的小鼠在缺血性卒中后血脑屏障(BBB)通透性增加低于野生型对照小鼠，提示uPAR通过增加血脑屏障通透性而加重缺血性脑损伤。此外，作为机制，我们发现，缺血损伤后血脑屏障通透性的增加与预先存在的血管的通透性增加有关，但在损伤1周时观察到的损伤内通透性的增加与新生的血管有关，而新生血管与星形胶质细胞不相互作用。

In the present study we observed that mice with gene deficient of uPAR had lower blood-brain barrier(BBB) permeability increase after ischemic stroke than their wild type control, suggesting that uPAR deteriorates ischemic brain damage via increase in BBB permeability. In addition, as mechanisms, we found that the increase in the BBB permeability just after ischemic damage was associated with the increase in the permeability of preexisting vessels but the increase in the permeability observed inside of damage at 1 week was associated with newly generated vessels which did not interact with astrocytes.