LE3 .A278 2009

2009

Wilson, Brian

Acadia University

Bachelor of Science with Honours in Biology

Honours

Biology

Biology

Relaxin is a peptide hormone belonging to the insulin peptide super family. Previous research has demonstrated that relaxin has neuroprotective effects that decrease cell death and damage during ischemic stroke. Many of these neuroprotective mechanisms such as vasodilation, suppression of inflammation, and activation of nitric oxide synthase pathways, involve genes whose expression is controlled by a family of transcription factors called Hypoxia Inducible Factors (HIFs). Active HIF complexes are primarily down-regulated by posttranscriptional degradation of the alpha subunit, Hypoxia Inducible Factor -1 alpha (HIF-1), under normoxic conditions. This study investigates the possibility that relaxin enhances natural cellular defences during ischemia by stimulating the expression of HIF- 1 or by suppressing its posttranscriptional degradation. An organotypic neonatal rat brain culture system was used. Cultured slices were divided into four treatment groups: relaxin treatment under normoxia, relaxin treatment under ischemia, no relaxin treatment under ischemia and no relaxin treatment under normoxia. Brain tissue from each treatment group was paraffin-embedded and immunostained for HIF-1. Qualitative analysis revealed clear and consistent immunopositive staining for HIF-1 in slices exposed to ischemic conditions as expected. There was no obvious increase in HIF-1 immunoactivity between the relaxin-treated and untreated ischemic groups to suggest that relaxin stimulates HIF-1 expression during ischemia. However, HIF-1 was expressed in relaxin treated slices not exposed to ischemia which suggests that relaxin may induce HIF-1 expression through a non-hypoxic related pathway. Further investigation is needed to better quantify and analyse these findings.

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https://scholar.acadiau.ca/islandora/object/theses:588