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Differential Expression Patterns of Gangliosides in the Ischemic Cerebral Cortex Produced by Middle Cerebral Artery Occlusion  

Kwak, Dong Hoon (Department of Biological Science, College of Natural Sciences, Wonkwang University)
Kim, Sung Min (Department of Biological Science, College of Natural Sciences, Wonkwang University)
Lee, Dea Hoon (Department of Biological Science, College of Natural Sciences, Wonkwang University)
Kim, Ji Su (Department of Biological Science, College of Natural Sciences, Wonkwang University)
Kim, Sun Mi (Department of Biological Science, College of Natural Sciences, Wonkwang University)
Lee, Seo Ul (Department of Pharmacology, Wonkwang University School of Medicine)
Jung, Kyu Yong (Department of Pharmacology, Wonkwang University School of Medicine)
Seo, Byoung Boo (Department of Molecular and Experimental Medicine, The Scripps Research Institute)
Choo, Young Kug (Department of Biological Science, College of Natural Sciences, Wonkwang University)
Abstract
Neuronal damage subsequent to transient cerebral ischemia is a multifactorial process involving several overlapping mechanisms. Gangliosides, sialic acid-conjugated glycosphingolipids, reduce the severity of acute brain damage in vitro. However their in vivo effects on the cerebral cortex damaged by ischemic infarct are unknown. To assess the possible protective role of gangliosides we examined their expression in the cerebral cortex damaged by ischemic infarct in the rat. Ischemia was induced by middle cerebral artery (MCA) occlusion, and the resulting damage was observed by staining with 2, 3, 5-triphenylterazolium chloride (TTC). High-performance thin-layer chromatography (HPTLC) showed that gangliosides GM3 and GM1 increased in the damaged cerebral cortex, and immunofluorescence microscopy also revealed a significant change in expression of GM1. In addition, in situ hybridization demonstrated an increase in the mRNA for ganglioside GM3 synthase. These results suggest that gangliosides GM1 and GM3 may be synthesized in vivo to protect the cerebral cortex from ischemic damage.
Keywords
Cerebral Cortex; Gangliosides; HPTLC; Ischemia; Monoclonal Antibody;
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