title: Immunohistochemical expression of fibroblast growth factor (FGF)-2 in epilepsy-associated malformations of cortical development (MCDs).
abstract: To elucidate the biological significance of dysplastic cells in malformations of cortical development, an immunohistochemical study was performed to investigate fibroblast growth factor-2 (FGF-2) expression in corticectomy specimens from epilepsy patients, including focal cortical dysplasia (FCD) with balloon cells (BCs) (n=4; age/sex=2M, 14F, 24M, 45M), tubers of tuberous sclerosis complex (TSC-tubers) (n=2; 1F, 3F), FCD without BCs (n=3; 23F, 23M, 25M), and gliotic lesions (n=3; 12M, 25M, 29M). The nucleus and/or cytoplasm of astrocytes in all cases examined were positive for FGF-2; however, FGF-2 immunoreactivity was not detected in oligodendroglial cells. In all dysplastic lesions, FGF-2 was detected in the astrocytic nuclei, and cytoplasm and/or nuclei of BCs. Dysplastic neurons (DNs) in FCD with BCs and TSC-tubers were variably positive for FGF-2 in the cytoplasm, but FGF-2 was not detected in the neurons of FCD without BCs. The number of FGF-2 immunoreactive cells (FGF-2-IR%) in FCD with BCs (46.0+/-4.1%) was higher than that in FCD without BCs (19.8+/-3.1%) and gliotic lesions (19.5+/-3.3%) with statistical significance (P<0.001). These results, together with previous reports showing FGF-2 expression in neuroblasts and glioblasts in human fetal brain, and mainly in astrocytes in adult brain, suggest that FGF-2 expression in MCDs reflects incomplete differentiation and maturation of dysplastic cells, and that FGF-2-IR% is associated with histological subtypes of MCD, reflecting the timing of insults underlying the pathogenesis of each disorder.
authors.affiliation: Department of Child Neurology, Institute of Neurological Sciences, Faculty of Medicine, Tottori University, Yonago, Tottori, Japan.
authors.forename: Chitose
authors.initials: C
authors.lastname: Sugiura
authors.forename: Hajime
authors.initials: H
authors.lastname: Miyata
authors.forename: Manami
authors.initials: M
authors.lastname: Ueda
authors.forename: Eisaku
authors.initials: E
authors.lastname: Ohama
authors.forename: Harry V
authors.initials: HV
authors.lastname: Vinters
authors.forename: Kousaku
authors.initials: K
authors.lastname: Ohno
mesh_terms: D000293:Adolescent; D000328:Adult; D001253:Astrocytes / Q000378:metabolism; D051792:Basic Helix-Loop-Helix Proteins / Q000096:biosynthesis; D002540:Cerebral Cortex / Q000002:abnormalities* / Q000378:metabolism*; D002648:Child; D002675:Child, Preschool; D004827:Epilepsy / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D005260:Female; D016222:Fibroblast Growth Factor 2 / Q000096:biosynthesis*; D006801:Humans; D007150:Immunohistochemistry; D007223:Infant; D008297:Male; D054220:Malformations of Cortical Development / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D008875:Middle Aged; D009419:Nerve Tissue Proteins / Q000096:biosynthesis; D000076104:Oligodendrocyte Transcription Factor 2; D009836:Oligodendroglia / Q000378:metabolism
chemical_list: D051792:Basic Helix-Loop-Helix Proteins; D016222:Fibroblast Growth Factor 2; D009419:Nerve Tissue Proteins; D000076104:Oligodendrocyte Transcription Factor 2; C405708:OLIG2 protein, human