Proteomic analysis of human cerebral cortex in epileptic patients
Epilepsy affects more than 0.5% of the world population and is known to be associated with a large genetic component eliciting an electrical hyperexcitability in the central nervous system. However, its pathogenic mechanisms remain poorly understood. In order to gain greater molecular incite in the...
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Published in: | Experimental & molecular medicine pp. 185 - 191 |
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Main Authors: | , , |
Format: | Journal Article |
Language: | Korean |
Published: |
생화학분자생물학회
01-04-2004
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Subjects: | |
Online Access: | Get full text |
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Summary: | Epilepsy affects more than 0.5% of the world
population and is known to be associated with a
large genetic component eliciting an electrical hyperexcitability
in the central nervous system.
However, its pathogenic mechanisms remain poorly
understood. In order to gain greater molecular
incite in the pathogenesis in epilepsy, we analyzed
proteomes of human cerebral cortices. Quantitative
proteome analysis was used to compare signals
corresponding to individual proteins between
epileptic cerebral cortices from patients with temporal
lobe epilepsy and age-matched non-epileptic
subjects. To minimize individual variations, gender
and age of the patients were matched. Changes
of several spots were consistent among 6 pairs
of epileptic patients and nonepileptic subjects.
One of the spots was identified as the mitochondrial
type Mn-superoxide dismutase (Mn-SOD) confirmed
by Western blot analysis with Mn-SOD
antibody and enzyme activity assay. Such results
were agreeable with chemical and physical parameters
given by the 2-dimensional electrophoresis
(2-DE) gel. Mn-SOD was consistently down-regulated
in epileptic cerebral cortices compared with
those of nonepileptic subjects. Our results demonstrate
a clear link between pathogenesis of epilepsy
and SOD. Additionally, we identified four
proteins that were consistently over-expressed in
all epileptic temporal neocortices specimens and
the other four proteins that were found to be expressed
less than non-epileptic control subjects.
These proteomic data provide cellular markers in
the understanding mechanism of the epilepsy pathogenesis. KCI Citation Count: 25 |
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Bibliography: | G704-000088.2004.36.2.006 http://kmbase.medric.or.kr/Main.aspx?d=KMBASE&m=VIEW&i=0620920040360020185 |
ISSN: | 1226-3613 2092-6413 |