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Relaxin, cerebral edema and the pathophysiology of stroke in rats

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Title: Relaxin, cerebral edema and the pathophysiology of stroke in rats
Author: Bergeron, Lindsay
Department: Department of Biomedical Sciences
Program: Biomedical Sciences
Advisor: Summerlee, Alastair
Abstract: This thesis investigates the protective effects of relaxin peptides in ischemic stroke. Previous studies have shown that relaxin protects tissue from ischemic damage through initiation of multiple mechanisms, which may affect numerous pathophysiological events that are initiated after ischemic stroke. A relaxin paralog, relaxin-3, is found primarily in the central nervous system. The ability of relaxin-3 to provide protection to tissues under ischemic stress has not yet been explored although the abundant cerebral expression of this peptide and its native receptor make it a logical target for study. This thesis sets out to assess the protective effects upon relaxin peptide administration and aims to identify the mechanisms responsible for any observed protective effects using both in vitro and in vivo ischemic stroke models. The first set of experiments demonstrates that relaxin-3 is as effective in protecting the brain from the deleterious effects of ischemic stroke as is observed with relaxin treatment. These data also implicate cellular protection as a mechanism contributing to the overall defenses observed with relaxin treatment. The second set of experiments exhibit the ability of relaxin peptides to alter the myogenic reactivity of rat middle cerebral arteries. The ability of relaxins to modulate smooth muscle function may make these peptides promising candidates for vascular protection in ischemic stroke. Data from the third set of experiments suggest that relaxin peptides reduce the development of cytotoxic edema after ischemic stroke by modulating AQP4 levels on astrocyte foot processes in the peri-infarct area. Overall, this thesis presents protective mechanisms involved in the overall protection provided by relaxin administration. This research promises to increase our understanding of the role that relaxin peptides play in limiting damage to brain tissue during ischemia and raises an intriguing possibility for a therapeutic use of relaxin in ischemic stroke.
URI: http://hdl.handle.net/10214/7832
Date: 2014-01
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