2016
DOI: 10.1016/j.neuroscience.2016.10.034
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Thrombin and protein C pathway in peripheral nerve Schwann cells

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Cited by 20 publications
(23 citation statements)
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“…Elevation of thrombin is in-line with previously observed nervous system disease models such as stroke [23], mild-traumatic brain injury (mTBI) [24], nerve crush [25] and the finding that thrombin activity influences synaptic function [24,2628].…”
Section: Discussionsupporting
confidence: 82%
“…Elevation of thrombin is in-line with previously observed nervous system disease models such as stroke [23], mild-traumatic brain injury (mTBI) [24], nerve crush [25] and the finding that thrombin activity influences synaptic function [24,2628].…”
Section: Discussionsupporting
confidence: 82%
“…Nexin-1, instead, a member of the large serpin superfamily, directly inhibits thrombin proteolytic activity (Cavanaugh et al, 1990; Gurwitz and Cunningham, 1990). In injured sciatic nerves, thrombin levels are elevated immediately after damage and reach their peak 1 day post-injury, declining after one week (Smirnova et al, 1996; Gera et al, 2016). On the contrary, upregulation of Nexin-1 in injured nerves occurs 6–9 days after thrombin induction (Meier et al, 1989; Smirnova et al, 1996) and is required to neutralize excessive thrombin proteolytic activity.…”
Section: Plasminogen Activators and Related Proteasesmentioning
confidence: 99%
“…In ischemic and hemorrhagic stroke, microglia are recruited to the site of injury where they mediate neuronal death [ 54 ] and contribute to brain recovery [ 44 ]. In these settings, the upregulated brain concentrations of thrombin have been linked to neuronal damage [ 26 , 29 , 30 , 55 , 56 ]. In Alzheimer's disease and in vascular dementia, high levels of thrombin and other coagulation factors have been detected in the brain aside with the recruitment of microglia and additional inflammatory components [ 57 59 ].…”
Section: Discussionmentioning
confidence: 99%