Relaxin production during cerebral ischemia and its potential role in neuroprotection
LE3 .A278 2010
2010
Wilson, Brian
Acadia University
Bachelor of Science
Honours
Biology
The peptide hormone relaxin, a member of the insulin superfamily, has a variety of effects in mammalian organs. Evidence suggests that relaxin is produced constitutively in cardiac cells, but there is an upregulation of production under ischemic stress which initiates cellular pathways that protect cardiomyocytes. Data from the brain mirrors these results as studies of cerebral ischemia have shown that injecting relaxin into the brain before an ischemic stress results in a reduction of the size of the damaged area. This study aims to determine whether relaxin is produced in the brain during ischemic stress, and its effectiveness in retaining tissue viability during ischemia- reperfusion. Neonatal rat brain slices were cultured and divided among four experimental groups: normoxic, hypoxic and each of these in combination with relaxin. Total RNA was collected from brain slices treated with normoxic and hypoxic media with the intent of using qPCR to measure relative expression of the relaxin gene. Relaxin primers were designed and tested with rat brain cDNA and optimization trials were conducted with qPCR studies ongoing. Normoxic and hypoxic treated brain slices were processed for immunohistochemical analysis of relaxin protein expression. Immunofluorescence in slices from both treatment groups was similar suggesting that relaxin protein expression was not upregulated under ischemic conditions. Using spectroscopy, cultured brain slices in normoxic, hypoxic and hypoxic + relaxin conditions were compared to map progressive ischemic damage over time. Initial data suggests there is an absorbance signature associated with ischemic tissue that may permit the use of spectroscopy to track ischemia- related changes however, relaxin treatment had no effect on this signature. Future research will determine the mechanisms behind relaxin- induced neuroprotection.
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https://scholar.acadiau.ca/islandora/object/theses:746
