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. 2016 Jan 25;10:2. doi: 10.3389/fncel.2016.00002

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Copyright © 2016 Suzuki, Nagai and Umemura.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution and reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic of the mechanisms of the increase in BBB permeability by recombinant tissue-type plasminogen activator (rt-PA) treatment after ischemic stroke. rt-PA activates the low-density lipoprotein receptor-related protein (LRP), which is upregulated in endothelial cells (ECs) by ischemic stress (1). The activation of LRP induces the transcriptional upregulation of VEGF. Secreted VEGF binds to VEGFR-2 on the surface of ECs through an autocrine mechanism and induces its phosphorylation (3). The activation of VEGFR-2 leads to an increase in endocytosis and to the activation of LRP, resulting in enhanced BBB permeability by endocytosis and subsequent transcellular transport of proteins into cerebroparenchyma (4). Tyr, TJ.