Investigating PAI-1, ICAM-1, and VCAM-1 expression dependence on neural activity within the acute phase of stroke in mice endothelial cells

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dc.contributor.authorBurford, Samuel A.
dc.date.accessioned2026-02-04T20:11:29Z
dc.date.available2026-02-04T20:11:29Z
dc.date.issued2024
dc.description.abstractStroke is a leading cause of death and disability worldwide. Following an Ischemic stroke, of which 87% of all strokes are, a spreading depolarization occurs, propagating damage to healthy tissue. Through initial experimentation, the procoagulant protein Plasminogen Activator Inhibitor-1 (PAI-1) displayed a unique expression pattern 24 hours following an ischemic stroke model in mice, producing a localized region of expression within endothelial cells contralateral to the stroke site. Through the application of a strong GABA agonist and using a passive diffusion method to limit tissue damage, my goal was to determine if the neural activity of the spreading depolarization was responsible for PAI-1 expression. I also aimed to observe expression patterns of Intracellular Adhesion Molecule-1 (ICAM-1) and Vascular Cell Adhesion Molecule-1 (VCAM-1) using immunolabelling. Expression of PAI-1 through immunolabelling was inconclusive due to high levels of endogenous binding of the secondary antibody. An attempt to limit endogenous binding was unsuccessful. VCAM-1 imaging did not display significant expression, however ICAM-1 did display a stroke dependent expression, in a pattern where proximity to the stroke site was indicative of total expression. Though PAI-1 expression manipulation was inconclusive, the potential for neural dependency in its expression remains. ICAM-1 expression results indicate a correlation between ICAM-1 expression and inflammation following stroke and likely does not display any neural activity dependence. If neural activity dependence can be further investigated in PAI-1, along with the identification of a potential neurovascular coupling pathway, then the expression of other vascular proteins may be studied to better understand the implications and reach of spreading depolarizations, along with the potential damage or resilience they may provide.
dc.description.reviewstatusUnreviewed
dc.description.scholarlevelUndergraduate
dc.identifier.urihttps://hdl.handle.net/1828/23124
dc.language.isoen
dc.subject.departmentDepartment of Biology
dc.titleInvestigating PAI-1, ICAM-1, and VCAM-1 expression dependence on neural activity within the acute phase of stroke in mice endothelial cells
dc.typeHonours thesis

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