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• W1994653861 abstract "We have studied the involvement of the thrombin receptor [protease-activated receptor-1 (PAR-1)] in astrogliosis, because extravasation of PAR-1 activators, such as thrombin, into brain parenchyma can occur after blood-brain barrier breakdown in a number of CNS disorders. PAR1 - / - animals show a reduced astrocytic response to cortical stab wound, suggesting that PAR-1 activation plays a key role in astrogliosis associated with glial scar formation after brain injury. This interpretation is supported by the finding that the selective activation of PAR-1 in vivo induces astrogliosis. The mechanisms by which PAR-1 stimulates glial proliferation appear to be related to the ability of PAR-1 receptor signaling to induce sustained extracellular receptor kinase (ERK) activation. In contrast to the transient activation of ERK by cytokines and growth factors, PAR-1 stimulation induces a sustained ERK activation through its coupling to multiple G-protein-linked signaling pathways, including Rho kinase. This sustained ERK activation appears to regulate astrocytic cyclin D1 levels and astrocyte proliferation in vitro and in vivo . We propose that this PAR-1-mediated mechanism underlying astrocyte proliferation will operate whenever there is sufficient injury-induced blood-brain barrier breakdown to allow extravasation of PAR-1 activators." @default.
• W1994653861 created "2016-06-24" @default.
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• W1994653861 date "2005-04-27" @default.
• W1994653861 modified "2023-10-10" @default.
• W1994653861 title "Activation of Protease-Activated Receptor-1 Triggers Astrogliosis after Brain Injury" @default.
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• W1994653861 doi "https://doi.org/10.1523/jneurosci.5200-04.2005" @default.
• W1994653861 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6725104" @default.
• W1994653861 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15858058" @default.
• W1994653861 hasPublicationYear "2005" @default.

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