| Abstract No.: | B-C2086 |
| Country: | Canada |
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| Title: | CEREBRAL ISCHEMIA INDUCES MOUSE BRAIN SIALIDASE EXPRESSION AND ACTIVITY RESULTING IN ALTERED SYNAPTIC GLYCOPROTEIN SIALYATION. |
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| Authors/Affiliations: | 1 Will Costain*; 1 Ingrid Rasquinha; 1 Caitlin Jones; 1 Pernilla Berin; 1 Warren Wakarchuk;
1 NRC - Institute for Biological Science, Ottawa, ON, Canada
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| Content: | Central nervous system neurons are highly susceptible to ischemic damage. Cerebral ischemia is known to induce numerous alterations in gene and protein expression that are involved in mediating neuronal cell death and brain remodeling. Furthermore, cerebral ischemia induces dramatic and rapidly reversible structural changes in dendritic spine morphology that precede delayed post-ischemic neuronal death. This suggests that synaptic stress may initiate signals that propagate toward the cell body and instigate delayed cell death through a process described as synaptic apoptosis. Extracellular and neuronal membrane glycoproteins are commonly modified with glycans that possess a terminal sialic acid residue. Objectives: Here we have characterized the effect of cerebral ischemia on brain sialidase expression and activity. Additionally, we examined the effects of cerebral ischemia on the levels of synaptosomal glycoprotein sialyation. Materials, Methods and Results: Samples were prepared from contralateral (CT) and ipsilateral (ISC) hemispheres from adult male C57 mice subjected to a transient (60 min) middle cerebral artery occlusion (MCAO) followed by 3 - 20 hrs of reperfusion. QPCR experiments revealed that the expression of Neu1 was significantly increased in ISC brain. Although no significant differences in Neu1 protein levels were detected, ISC brain sialidase activity was significantly increased. CT and ISC synaptosomal proteins were separated using 2D PAGE gels and transferred to nitrocellulose. Sialic acid specific biotin conjugated lectins (SNA I and MAL II) were used to identify synaptosomal sialo-proteins. Numerous sialic acid containing glycoproteins were detected in synaptosomes. Finally, cerebral ischemia induced numerous alterations in synaptosomal sialo-protein expression as well as glycosylation. Conclusion: The results presented here indicate that cerebral ischemia affects the levels of synaptic sialic acid containing proteins and that this effect is likely to be related to alterations in sialidase activity. |
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