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Annie Meiniel - One of the best experts on this subject based on the ideXlab platform.
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the secretory Ependymal cells of the subcommissural organ which role in hydrocephalus
The International Journal of Biochemistry & Cell Biology, 2007Co-Authors: Annie MeinielAbstract:Abstract Ependyma in the central nervous system gives rise to several specialized cell types, including the secretory Ependymal cells located in the subcommissural organ. These elongated cells show large cisternae in their cytoplasm, which are filled with material secreted into the cerebrospinal fluid and toward the leptomeningeal spaces. A specific secretion of the subcommissural organ was named SCO-spondin, regarding its marked homology with developmental proteins of the thrombospondin superfamily (presence of thrombospondin type 1 repeats). The Ependymal cells of the subcommissural organ and SCO-spondin secretion are suspected to play a crucial role in cerebrospinal fluid flow and/or homeostasis. There is a close correlation between absence of the subcommissural organ and hydrocephalus in rat and mouse strains exhibiting congenital hydrocephalus, and in a number of mice transgenic for developmental genes. The Ependymal cells of the subcommissural organ are under research as a key factor in several developmental processes of the central nervous system.
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the secretory Ependymal cells of the subcommissural organ which role in hydrocephalus
The International Journal of Biochemistry & Cell Biology, 2007Co-Authors: Annie MeinielAbstract:Abstract Ependyma in the central nervous system gives rise to several specialized cell types, including the secretory Ependymal cells located in the subcommissural organ. These elongated cells show large cisternae in their cytoplasm, which are filled with material secreted into the cerebrospinal fluid and toward the leptomeningeal spaces. A specific secretion of the subcommissural organ was named SCO-spondin, regarding its marked homology with developmental proteins of the thrombospondin superfamily (presence of thrombospondin type 1 repeats). The Ependymal cells of the subcommissural organ and SCO-spondin secretion are suspected to play a crucial role in cerebrospinal fluid flow and/or homeostasis. There is a close correlation between absence of the subcommissural organ and hydrocephalus in rat and mouse strains exhibiting congenital hydrocephalus, and in a number of mice transgenic for developmental genes. The Ependymal cells of the subcommissural organ are under research as a key factor in several developmental processes of the central nervous system.
Harvey B. Sarnat - One of the best experts on this subject based on the ideXlab platform.
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Regional Ependymal Upregulation of Vimentin in Chiari II Malformation, Aqueductal Stenosis, and Hydromyelia
Pediatric and Developmental Pathology, 2004Co-Authors: Harvey B. SarnatAbstract:Vimentin, glial fibrillary acidic protein (GFAP) and S-100 β protein were studied by immunocytochemistry in the Ependyma of patients with Chiari II malformations, congenital aqueductal stenosis, and hydromyelia. Paraffin sections of brains and spinal cords of 16 patients were examined, 14 with Chiari II malformations, most with aqueductal stenosis and/or hydromyelia as associated features, and 2 patients with congenital aqueductal stenosis without Chiari malformation. Patients ranged in age from 20-wk gestation to 48 years. The results demonstrated: 1) in the fetus and young infant with Chiari II malformations, congenital aqueductal stenosis, and hydromyelia, vimentin is focally upregulated in the Ependyma only in areas of dysgenesis and not in the Ependyma throughout the ventricular system; 2) GFAP and S-100β protein are not coexpressed, indicating that the selective upregulation of vimentin is not simple maturational delay; 3) vimentin upregulation also is seen in the Ependymal remnants of the congenital atretic cerebral aqueduct, not associated with Chiari malformation; 4) in the older child and adult with Chiari II malformation, vimentin overexpression in the Ependyma becomes more generalized in the lateral ventricles as well, hence evolves into a nonspecific upregulation. The interpretation from these findings leads to speculation that it is unlikely that Ependymal vimentin is directly involved in the pathogenesis of Chiari II malformation, but may reflect a secondary upregulation due to defective expression of another gene. This gene may be one of rhombomeric segmentation that also plays a role in defective programming of the paraxial mesoderm for the basioccipital and supraoccipital bones resulting in a small posterior fossa. This interpretation supports the hypothesis of a molecular genetic defect, rather than a mechanical cause, as the etiology of the Chiari II malformation.
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histochemistry and immunocytochemistry of the developing Ependyma and choroid plexus
Microscopy Research and Technique, 1998Co-Authors: Harvey B. SarnatAbstract:The adult human Ependyma expresses no intermediate filament proteins or secretory proteins; the fetal Ependyma shows strong immunocytochemical (ICC) expression of vimentin, glial fibrillary acidic protein (GFAP), cytokeratins (CKs) of high molecular weight, glycoproteins, and S-100β protein. Each has a precise and specific spatial distribution within the developing Ependyma and a predictable time of appearance and regression in each region of the ventricular system. Several are coexpressed, but some appear earlier or persist longer than others. Secretory proteins of Ependymal cells are important in several developmental processes such as the guidance of axonal growth cones. GFAP is not expressed in the floor plate Ependyma at any stage of development, unlike vimentin and CK. The choroid plexus epithelium is a specialized Ependyma, with an ICC profile that differs from the surface Ependyma: vimentin, CK, and S-100β protein continue to be expressed throughout fetal and adult life, but GFAP is not expressed. Certain cerebral malformations are associated with specific ICC abnormalities: Ependymal S-100β protein continues to be immunoreactive in disorders of neuroblast migration; Ependymal vimentin is focally upregulated in Chiari malformations and congenital aqueductal stenosis. Other mammalian and nonmammalian species have characteristic profiles of Ependymal immunoreactivity to the same proteins expressed in humans but exhibit interspecific differences. Microsc. Res. Tech. 41:14–28, 1998. © 1998 Wiley-Liss, Inc.
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Ependymal abnormalities in lissencephaly pachygyria
Journal of Neuropathology and Experimental Neurology, 1993Co-Authors: Harvey B. Sarnat, Husam Darwish, Peter G. Barth, Cynthia L. Trevenen, Alfredo Pinto, Suresh Kotagal, Keiko Shishikura, Makiko Osawa, Rowena KorobkinAbstract:The Ependyma was examined in eight children with neuroblast migratory disorders of diverse origin: three cases of lissencephaly type 1 with severe to mild degrees of agyria/pachygyria, four cases of lissencephaly type 2 in Fukuyama muscular dystrophy and the Walker-Warburg syndrome, and one case of hemimegalencephalic pachygyria. Morphological and immunohistochemical abnormalities of the Ependyma were strikingly similar in all. Discontinuities were disproportionate to the degree of ventriculomegaly. In some regions, the Ependyma remained a pseudostratified columnar epithelium, though basal processes were absent. The poles of the horns of the lateral ventricles were replaced by extensive heterotopic Ependymal rosettes. Rosettes and rows of Ependyma also were in other subventricular sites. SubEpendymal nodules of large astrocytes and their processes bulged into the ventricular lumen after infancy. Ependymal cells did not express glial fibrillary acidic protein, but showed persistent expression of S-100 protein, cytokeratin CK-904 and sometimes vimentin long after these proteins normally disappear. An abnormal Ependyma in lissencephaly/pachygyria may contribute to disturbances in neuronogenesis, guidance of axonal projections and neuroblast migrations; it may be a primary factor in pathogenesis.
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Ependymal abnormalities in lissencephaly/pachygyria.
Journal of neuropathology and experimental neurology, 1993Co-Authors: Harvey B. Sarnat, Husam Darwish, Peter G. Barth, Cynthia L. Trevenen, Alfredo Pinto, Suresh Kotagal, Keiko Shishikura, Makiko Osawa, Rowena KorobkinAbstract:The Ependyma was examined in eight children with neuroblast migratory disorders of diverse origin: three cases of lissencephaly type 1 with severe to mild degrees of agyria/pachygyria, four cases of lissencephaly type 2 in Fukuyama muscular dystrophy and the Walker-Warburg syndrome, and one case of hemimegalencephalic pachygyria. Morphological and immunohistochemical abnormalities of the Ependyma were strikingly similar in all. Discontinuities were disproportionate to the degree of ventriculomegaly. In some regions, the Ependyma remained a pseudostratified columnar epithelium, though basal processes were absent. The poles of the horns of the lateral ventricles were replaced by extensive heterotopic Ependymal rosettes. Rosettes and rows of Ependyma also were in other subventricular sites. SubEpendymal nodules of large astrocytes and their processes bulged into the ventricular lumen after infancy. Ependymal cells did not express glial fibrillary acidic protein, but showed persistent expression of S-100 protein, cytokeratin CK-904 and sometimes vimentin long after these proteins normally disappear. An abnormal Ependyma in lissencephaly/pachygyria may contribute to disturbances in neuronogenesis, guidance of axonal projections and neuroblast migrations; it may be a primary factor in pathogenesis.
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role of human fetal Ependyma
Pediatric Neurology, 1992Co-Authors: Harvey B. SarnatAbstract:Fetal Ependyma is an active secretory structure for the programming of developmental events, including the arrest of neuronogenesis, the guidance of axonal growth cones, motor neuron differentiation, and probably also the maintenance and transformation of radial glial cells that guide migratory neuroblasts. The floor plate, induced by the notochord, is the first part of the neuroepithelium to differentiate. It establishes polarity and growth gradients of the neural tube and has immunohistochemical features that differ from all other regions of the Ependyma. The dorsal and ventral median septa, formed by floor and roof plate Ependymal processes, prevent aberrant decussations of developing long tracts, but permit the passage of commissural axons. Fetal Ependyma synthesizes several intermediate filament proteins absent from mature Ependymal cells, although some are also expressed in undifferentiated neuroepithelial cells. Fetal Ependyma also produces diffusible molecules, such as neural cell adhesion molecule, proteoglycans, nerve growth factor, and S-100 protein, all in specific temporal and spatial distributions. Maturation of the Ependyma is not complete until the postnatal period. An abnormal fetal Ependyma may play a primary role in the pathogenesis of some cerebral malformations, such as lissencephaly/pachygyria and holoprosencephaly.
Jens D Mikkelsen - One of the best experts on this subject based on the ideXlab platform.
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central innervation of the rat Ependyma and subcommissural organ with special reference to ascending serotoninergic projections from the raphe nuclei
The Journal of Comparative Neurology, 1997Co-Authors: Jens D Mikkelsen, Anders Hayschmidt, Philip J LarsenAbstract:: The subcommissural organ (SCO) and the cerebral Ependyma receive serotoninergic innervation, but little is known about their origin in the raphe nuclei. Application of the retrograde tracer cholera toxin subunit B (ChB) in the third ventricle resulted in uptake in Ependymal axons and backfilling of perikarya in the dorsomedian part of the dorsal raphe nucleus, immediately under the caudal aqueduct. By using dual staining with antisera against serotonin and ChB, a portion of the retrogradely labeled neurons was observed to co-store serotonin. Phaseolus vulgaris-leucoagglutinin (PHA-L) was injected into different raphe nuclei to fill the neurons in the same areas where the retrogradely labeled neurons were found. PHA-L injection in the midline of the dorsal raphe nucleus gave rise to ascending axonal processes in the mesencephalic central gray, from where they entered the periventricular strata and the third ventricular Ependyma. In the cerebral Ependyma, large numbers of positive fibers were consistently found in the ventral part of the lateral ventricles and in the dorsal part of the third ventricle. A large number of PHA-L-immunoreactive fibers were observed in the hypendymal layer of the lateral part of the SCO. Terminal fibers near the Ependymal cells were also observed. In all cases, the PHA-L injections labeled innervating fibers both within the Ependyma and in the SCO, whereas injections into the median raphe nucleus or in other raphe nuclei (i.e., the raphe pallidus and the raphe pontis) labeled fibers neither in the SCO nor in the Ependyma. This study shows that a specific group of predominantly serotoninergic neurons innervates both the Ependyma and the SCO and is probably involved in cerebrospinal fluid regulation.
Patrizia Ferretti - One of the best experts on this subject based on the ideXlab platform.
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Up-regulation of neural stem cell markers suggests the occurrence of dedifferentiation in regenerating spinal cord
Development Genes and Evolution, 2003Co-Authors: Sally Walder, Fang Zhang, Patrizia FerrettiAbstract:Following tail amputation in urodele amphibians, an Ependymal tube, that resembles a developing neural tube, forms from Ependymal cells that migrate from the cord stump and elongates by cell proliferation. Expression of the keratin pair 8 and 18 has been observed in the developing urodele nervous system and is maintained in the Ependymal cells of the mature cord. We show here that expression of these keratins is not unique to urodeles, but is also observed in the radial glia of the human spinal cord, suggesting that these proteins might play a role both in neural development and regeneration. Analysis of their expression in the regenerating spinal cord following tail amputation shows that their expression, as well as that of glial fibrillary acidic protein (GFAP), is maintained in the Ependymal tube during regeneration, though differences in their levels of expression are observed along the anteroposterior axis and appear to be related to the progression of morphogenesis. In addition, we show that following tail amputation the Ependymal tube expresses the neural stem cell markers nestin and vimentin, which are undetectable in normal urodele spinal cord. This up-regulation of neural stem cell markers shows that the Ependymal cells undergo a phenotypic change. Whereas maintenance of keratin and GFAP expression in the adult Ependyma may reflect a higher plasticity of these cells in adult urodeles than in other vertebrates, re-expression of markers of early neural development suggests the occurrence of a dedifferentiation process in the spinal cord in response to injury.
L. E. Becker - One of the best experts on this subject based on the ideXlab platform.
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overexpression of nestin and vimentin in the Ependyma of spinal cords from hydrocephalic infants
Neuropathology and Applied Neurobiology, 1997Co-Authors: Tomoyuki Takano, L. E. BeckerAbstract:The Ependyma of the spinal central canal in cases of hydrocephalus shows abnormalities which vary with the aetiology of ventricular dilatation. To determine whether these Ependymal changes are developmental or reactive in nature, immunohistochemical findings were compared between nine normal controls and 12 cases of hydrocephalus (three each of congenital aqueductal stenosis, Dandy-Walker malformation, Chiari type II malformation, and post-haemorrhagic hydrocephalus) using antisera to nestin, vimentin and glial fibrillary acidic protein. The main pathological findings were disruption of Ependymal layer, apparent pseudostratification of Ependyma, expansion, cleft or syrinx formation in relation to the central canal, and Ependymal rosette formation. In normal developing fetal spinal cord, nestin and vimentin were expressed mainly in pseudostratified Ependymal cells and radial fibres in the median septum. In cases with congenital hydrocephalus (congenital aqueductal stenosis, Dandy-Walker malformation, and Chiari type II malformation), nestin was overexpressed in immature Ependymal cells, and strong vimentin immunoreactivity was detected in the long tract of radial fibres in the median septum. Nestin and vimentin were also expressed in small cells and their fibres which covered areas denuded of Ependymal cells in cases of Chiari type II malformation and post-haemorrhagic hydrocephalus. Two conclusions are suggested by this report. First, the Ependyma of the spinal central canal in congenital hydrocephalus shows a delay in maturation of radial glial cells into mature astrocytes and Ependymal cells. Second, areas of Ependymal denudation may be repaired by the immature glial cells derived from subEpendymal cells.
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Overexpression of nestin and vimentin in Ependymal cells in hydrocephalus
Acta Neuropathologica, 1996Co-Authors: Tomoyuki Takano, James T. Rutka, L. E. BeckerAbstract:In order to elucidate the immunohistochemical features of hydrocephalic Ependyma, immunohistochemical examination was undertaken in 11 normal, post-mortem brains (age range, 11 weeks’ postconception to 6 months after birth) and 12 hydrocephalic brains (three cases each of congenital aqueductal stenosis, Dandy-Walker malformation, Arnold-Chiari type II malformation and posthemorrhagic hydrocephalus) by using antisera to nestin, vimentin and glial fibrillary acidic protein (GFAP). In normal brains, nestin was predominantly expressed in neuroepithelial cells and radial glial fibers during the period of neuronal migration. Vimentin immunoreactivity was principally detected in immature Ependymal cells and their basal fibers after the period of neuronal migration, then partly replaced by GFAP reactivity during late gestation. In hydrocephalus, the areas of Ependymal disruption were covered with nestin- or vimentin-positive cells. Nestin and vimentin were also expressed in immature Ependymal cells or their basal processes in anatomical regions such as the roof or floor plate of the fourth ventricle or the cerebral aqueduct, and the ventral part of the third ventricle. These results suggest that the overexpression of nestin and vimentin in hydrocephalus follows two patterns: a reactive pattern of proliferating immature glial cells associated with Ependymal cell loss and an abnormal developmental pattern of immunopositivity associated with anatomical regions in the midline mesencephalon.