Urokinase-type Plasminogen Activator Promotes Synaptic Recovery In The Ischemic Brain

• Type of Material: Article
• Authors: Manuel Yepes, Emory University
• Language: English
• Date: 2018-03-20
• Publisher: Insight Medical Publishing
• Publication Version: Final Published Version
• Copyright Statement: © 2018 iMedPub LTD All rights reserved.
• License: Creative Commons Attribution 3.0 Unported
• Final Published Version (URL): http://dx.doi.org/10.21767/2573-5349.100016
• Title of Journal or Parent Work: Journal of Translational Neurosciences
• Volume: 03
• Issue: 02
• Grant/Funding Information: This work was supported in part by National Institutes of Health (NIH) Grants NS-091201 (to M.Y) and NS-079331 (to M.Y), and VA MERIT Award IO1BX003441 (to M.Y).
• Research Categories: Biology, Neuroscience

Abstract

Synaptic dysfunction underlies the development of neurological impairment following an acute ischemic stroke. Unfortunately, to this date there is no therapeutic approach to protect and repair the synapse that has suffered an ischemic injury. However, recent research with in vitro models of hypoxia, in vivo models of cerebral ischemia and different neuroradiological techniques has revealed that during the recovery phase from a hypoxic injury neurons release the serine proteinase urokinase-type plasminogen activator (uPA) and astrocytes recruit its receptor (uPAR) to their plasma membrane; and that binding of neuronal uPA to astrocytic uPAR promotes the recovery of the “tripartite synapse” that has suffered an acute ischemic injury. The translational relevance of these findings is underscored by the fact that intravenous treatment with recombinant uPA promotes synaptic recovery and functional improvement following an acute ischemic stroke.