Repair of the ependyma in hydrocephalic brains

Collins, Patricia; Fairman, S.

doi:10.1111/j.1365-2990.1990.tb00931.x

Cited by 19 publications

(8 citation statements)

References 17 publications

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“…Some of these nestin-and vimentinpositive cells were also GFAP-positive but, being small, they were probably not reactive astroglial cells. In experimental hydrocephalus induced by intracisternal kaolin injection, it is observed that the areas of ependymal disruption are filled with small round cells and fine processes before any response by reactive astrocytes occurs [5,6]. These small cells are ultrastructurally similar to glial precursor cells and are, therefore, thought to be derived from subependymal cells [18].…”

Section: Discussionmentioning

confidence: 99%

Overexpression of nestin and vimentin in the ependyma of spinal cords from hydrocephalic infants

Takano¹,

Becker²

1997

Neuropathol Appl Neurobiol

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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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Section: Discussionmentioning

confidence: 99%

Overexpression of nestin and vimentin in the ependyma of spinal cords from hydrocephalic infants

Takano¹,

Becker²

1997

Neuropathol Appl Neurobiol

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“…For the most part, there is a consistent sequence and array of pathologic changes that correlates with the degree of ventricular dilatation, including stretching, atrophy and focal loss of ependyma, periventricular edema, and subependymal gliosis. Although some ependymal cell proliferation has been reported as part of the overall tissue response (Clark and Milhorat, 1970;Page, 1975); repair of the deficit appears to be undertaken entirely by subependymal cells, with no evidence of their differentiation into ciliated ependyma cells (Bruni et al, 1985;Collins and Fairman, 1990;Margolis and Kilham, 1969;Sarnat 1995).…”

Section: Ependymal Proliferation-normalmentioning

confidence: 99%

Ependymal development, proliferation, and functions: A review

Bruni

1998

Microsc. Res. Tech.

243

129

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A survey of the literature shows that proliferation of ependyma occurs largely during the embryonic and early postnatal periods of development in most species. Differentiation of these cells proceeds along particular regional and temporal gradients as does the expression of various cytoskeletal (vimentin, cytokeratins, glial fibrillary acidic protein) and secretory proteins (S‐100). Turnover declines significantly postnatally, and only low levels of residual activity persist into adulthood under normal conditions. Although the reported response of ependyma to injury is somewhat equivocal, only limited regenerative capacity appears to exist and to varying degrees in different regions of the neuraxis. Proliferation has been most often observed in response to spinal cord injury. Indeed, the ependyma plays a significant role in the initiation and maintenance of the regenerative processes in the spinal cord of inframammalian vertebrates. In the human, however, ependyma appears never to regenerate at any age nor re‐express cytoskeletal proteins characteristic of immature cells. The functions of ependyma including tanycytes, a specialized form of ependymal cell that persists into adulthood within circumscribed regions of the nervous system, are still largely speculative. Fetal unlike mature ependyma is believed to be secretory and is believed to play a role in neurogenesis, neuronal differentiation/axonal guidance, transport, and support. In the adult brain, mature ependyma is not merely an inert lining but may regulate the transport of ions, small molecules, and water between the cerebrospinal fluid and neuropil and serve an important barrier function that protects neural tissue from potentially harmful substances by mechanisms that are still incompletely understood. Microsc. Res. Tech. 41:2–13, 1998 © 1998 Wiley‐Liss, Inc.

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“…Ependymal proliferation occurs after various brain injuries but it is insufficient to provide coverage where the ventricle surface has been denuded (Aikawa and Suzuki, 1986;Bernstein, 1986;Del Bigio and Bruni, 1986;Del Bigio and Bruni, 1988). Indeed, repair of ventricular surface lesions is largely a reaction of subependymal cells (Collins and Fairman, 1990).…”

Section: Proliferation and Growth Factorsmentioning

confidence: 99%

The ependyma: A protective barrier between brain and cerebrospinal fluid

Bigio

1995

Glia

286

182

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This review summarizes the current scientific literature concerning the ependymal lining of the cerebral ventricles of the brain with an emphasis on selective barrier function and protective roles for the common ependymal cell. Topics covered include the development, morphology, protein and enzyme expression including reactive changes, and pathology. Some cells lining the neural tube are committed at an early stage to becoming ependymal cells. They serve a secretory function and perhaps act as a cellular/axonal guidance system, particularly during fetal development. In the mature mammalian brain ependymal cells possess the structural and enzymatic characteristics necessary for scavenging and detoxifying a wide variety of substances in the CSF, thus forming a metabolic barrier at the brain-CSF interface.

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Repair of the ependyma in hydrocephalic brains

Cited by 19 publications

References 17 publications

Overexpression of nestin and vimentin in the ependyma of spinal cords from hydrocephalic infants

Overexpression of nestin and vimentin in the ependyma of spinal cords from hydrocephalic infants

Ependymal development, proliferation, and functions: A review

The ependyma: A protective barrier between brain and cerebrospinal fluid

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