Immunohistochemical analysis of developmental neural antigen expression in the balloon cells of focal cortical dysplasia

Abstract Balloon cells (BC) are the histological hallmarks of focal cortical dysplasia (FCD). Expression of the neural stem cell surface marker CD133 and other developmental markers was studied in the BC of FCD using formalin-fixed paraffin-embedded tissue from nine patients with FCD. Labeling index...

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Bibliographic Details
Published in:Journal of clinical neuroscience 2011-01, Vol.18 (1), p.114-118
Main Authors: Han, Chang-Woo, Min, Byung-Woo, Kim, Young, Jeong, Eun-Hui, Park, Chang-Soo, Woo, Young-Jong, Kim, Hyung-Seok, Lee, Min-Cheol
Format: Article
Language:English
Subjects:
AC133 Antigen
Adolescent
Adult
Antigens, CD - metabolism
Balloon cell
CD133 antigen
Child
Cortical dysplasia
Female
Frontal Lobe - metabolism
Frontal Lobe - pathology
Glycoproteins - metabolism
Humans
Immunohistochemistry
Intermediate Filament Proteins - metabolism
Male
Malformations of Cortical Development - metabolism
Malformations of Cortical Development - pathology
Middle Aged
Nerve Tissue Proteins - metabolism
Neuroglia - metabolism
Neuroglia - pathology
Neurology
Neurons - metabolism
Neurons - pathology
Peptides - metabolism
Stem cells
Temporal Lobe - metabolism
Temporal Lobe - pathology
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Summary:Abstract Balloon cells (BC) are the histological hallmarks of focal cortical dysplasia (FCD). Expression of the neural stem cell surface marker CD133 and other developmental markers was studied in the BC of FCD using formalin-fixed paraffin-embedded tissue from nine patients with FCD. Labeling indexes were calculated for all antibodies. BC were easily identified at the gray–white matter junction and they extended into the white matter. Immunoreactivity in BC was found for the following antigens in nine patients: CD133 (six patients; 22.2 ± 7.7%), CD34 (two patients; 0.4 ± 0.3%), nestin (nine patients; 37.6 ± 8.5%), vimentin (eight patients; 59.2 ± 8.7%), glial fibrillary acid protein (six patients; 34.3 ± 10.4%), microtubule-associated protein 2 (four patients; 8.3 ± 5.0%), neurofilament-middle/high (five patients; 10.2 ± 4.6%) and synaptophysin (three patients; 4.2 ± 3.3%). Neuronal nuclei (NeuN, neuron specific nuclear protein) was not expressed in BC of any patient. The results of this study suggest that BC in patients with FCD originate from glioneuronal precursor cells and that developmental defects of neuronal and glial specifications are important in the histogenesis of FCD.
ISSN:0967-5868
1532-2653
DOI:10.1016/j.jocn.2010.05.012