Heat shock proteins in the relaxin-induced protection of ischemic neural tissue
LE3 .A278 2010
2010
Wilson, Brian
Acadia University
Bachelor of Science
Honours
Biology
Relaxin is a peptide hormone with many diverse physiological actions. Although it was originally characterized as a pregnancy hormone, recent studies suggest that relaxin provides a variety of mammalian organs with protection against ischemia and reperfusion injury. Protection occurs through a variety of mechanisms such as oxygen free radical reduction, mast cell and neutrophil inhibition, vasodilation, and subsequent improvement of collateral circulation. In addition, it is possible that relaxin alters the production of heat shock proteins, which are part of the cellular stress response and function in the proper folding and transportation of proteins. The purpose of this study was to investigate the production of heat shock proteins in the relaxin- induced protection of neural tissue under ischemic stress. Organotypic slice cultures of neonatal rat brains were cultured over fourteen days and were then allocated to one of three media treatments: normoxic, hypoxic, and hypoxic and relaxin. Following treatment, slices were returned to normal culture conditions. At 6 and 12 hours post- treatment, slices were flash frozen or fixed and Hsp70 production was measured using immunohistochemistry. Ischemic slices that had been exposed to relaxin exhibited a reduction of Hsp70s, suggesting that relaxin suppresses the cellular stress response in neural tissue and possibly suppresses ischemic damage. Gene expression data from ongoing qPCR studies may corroborate our qualitative protein expression results. Stroke is currently the fourth leading cause of death in Canada, with 80% of cases resulting from ischemic stroke. This research may lead to therapies to ameliorate the effect of stroke.
The author retains copyright in this thesis. Any substantial copying or any other actions that exceed fair dealing or other exceptions in the Copyright Act require the permission of the author.
https://scholar.acadiau.ca/islandora/object/theses:734