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Results for “Neuroepithelial Cells”

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At least 19 recordsLinked to original sources

PubMed1997

Asymmetric division and polarity of neuroepithelial cells.

Neuroepithelial cells, the progenitors to the CNS neurons and glia, undergo both symmetric and asymmetric divisions. Symmetric divisions underlie the proliferation of neuroepithelial cells that predominates early in CNS development. Asymmetric divisions are thought to generate the cell types derived from neuroepithelial cells, such as neurons. Insight into the mechanism of asymmetric division of neuroepithelial cells has come from two lines of research, the study of their epithelial polarity and the analysis of the expression of vertebrate homologues of proteins known to be involved in cell fate determination in Drosophila.

Animals↗

PubMed2005

Long-term proliferation of human embryonic stem cell-derived neuroepithelial cells using defined adherent culture conditions.

Research on the cell fate determination of embryonic stem cells is of enormous interest given the therapeutic potential in regenerative cell therapy. Human embryonic stem cells (hESCs) have the ability to renew themselves and differentiate into all three germ layers. The main focus of this study was to examine factors affecting derivation and further proliferation of multipotent neuroepithelial (NEP) cells from hESCs. hESCs cultured in serum-deprived defined medium developed distinct tube structures and could be isolated either by dissociation or adherently. Dissociated cells survived to form colonies of cells characterized as NEP when conditioned medium from human hepatocellular carcinoma HepG2 cell line (MEDII) was added. However, cells isolated adherently developed an enriched population of NEP cells independent of MEDII medium. Further characterization suggested that they were NEP cells because they had a similar phenotype profile to in vivo NEP cells and expression SOX1, SOX2, and SOX3 genes. They were positive for Nestin, a neural intermediate filament protein, and Musashi-1, a neural RNA-binding protein, but few cells expressed further differentiation markers, such as PSNCAM, A2B5, MAPII, GFAP, or O4, or other lineage markers, such as muscle actin, alpha fetoprotein, or the pluripotent marker Oct4. Further differentiation of these putative NEP cells gave rise to a mixed population of progenitors that included A2B5-positive and PSNCAM-positive cells and postmitotic neurons and astrocytes. To proliferate and culture these derived NEP cells, ideal conditions were obtained using neurobasal medium supplemented with B27 and basic fibroblast growth factor in 5% oxygen. NEP cells were continuously propagated for longer than 6 months without losing their multipotent cell characteristics and maintained a stable chromosome number.

Animals↗

PubMed2003

Human neuroepithelial cells express NMDA receptors.

L-glutamate, an excitatory neurotransmitter, binds to both ionotropic and metabotropic glutamate receptors. In certain parts of the brain the BBB contains two normally impermeable barriers: 1) cerebral endothelial barrier and 2) cerebral epithelial barrier. Human cerebral endothelial cells express NMDA receptors; however, to date, human cerebral epithelial cells (neuroepithelial cells) have not been shown to express NMDA receptor message or protein. In this study, human hypothalamic sections were examined for NMDA receptors (NMDAR) expression via immunohistochemistry and murine neuroepithelial cell line (V1) were examined for NMDAR via RT-PCR and Western analysis. We found that human cerebral epithelium express protein and cultured mouse neuroepithelial cells express both mRNA and protein for the NMDA receptor. These findings may have important consequences for neuroepithelial responses during excitotoxicity and in disease.

Animals↗

PubMed1987

Cell cycle and neuroepithelial cell shape during bending of the chick neural plate.

Neuroepithelial cells change shape from spindle-like to wedge-like within three restricted areas (hinge points) of the bending neural plate. The mechanisms underlying these localized cell shape changes and the specific role that these changes play in bending are unclear. This study was designed to determine whether changes in neuroepithelial cell shape involve basal cellular expansion owing to alteration of the cell cycle. Neurulating chick embryos were treated with colchicine to arrest and accumulate cells in metaphase, and colchicine indices and cell generation times were calculated for the neural plate. During bending of the neural plate, cell generation time in the median hinge point, which contains predominantly wedge-shaped cells, was significantly longer than that in adjacent lateral areas of the neural plate, which contain predominantly spindle-shaped cells. In addition, cell generation time in the flat neural plate, which contains predominantly spindle-shaped cells and has not yet differentiated into the median hinge point and lateral subdivisions, was identical to that in lateral areas of the bending neural plate but was significantly shorter than that in the median hinge point. These results support the hypothesis that changes in neuroepithelial cell shape from spindle-like to wedge-like involve basal cellular expansion owing to alteration of the cell cycle. Additional tests of this hypothesis and studies on the role of localized cell shape changes in neurulation are in progress.

Animals↗

PubMed1977

The effect of LSD on the surface of neuroepithelial cells.

The neuroepithelial cells of 10 control chick embryos and of 22 exposed to lysergic acid diethylamide (LSD) (50 microgram/ml) were examined in scanning electron microscopy (SEM). In specimens exposed to LSD, the cells are swollen and their surface loses its cytoplasmic projections. Labelling techniques applied in transmission electron microscopy (TEM) show that ruthenium red attaches to the surface of the neuroepithelial cells in the form of a continuous dark line in both controls and treated specimens. However, when cationized ferritin or lanthanum is used, the label appears in the form of a continuous line in the controls whereas it is discontinuous in specimens exposed to LSD. These observations suggest that LSD alters the components of the neuroepithelial cell surface in the young chick embryo.

Animals↗

PubMed1999

Apoptotic cell death of proliferating neuroepithelial cells in the embryonic retina is prevented by insulin.

The role of programmed cell death is well established for connecting neurons. Conversely, much less is known about apoptosis affecting proliferating neuroepithelial cells. Chick retina from day 4 to day 6 of embryonic development (E), essentially proliferative, presented a defined distribution of apoptotic cells during normal in vivo development, as visualized by TdT-mediated dUTP nick end labelling (TUNEL). Insulin, expressed in the early chick embryonic retina as proinsulin, attenuated apoptosis in growth factor-deprived organotypic culture of E5 retina. This effect was demonstrated both by TUNEL and by staining of pyknotic nuclei, as well as by release of nucleosomes. Application of a 1 h [methyl-3H]thymidine pulse in ovo at E5, followed by organotypic culture in the presence or absence of insulin, showed that this factor alone decreased the degradation of labelled DNA to nucleosomes by 40%, as well as the proportion of labelled pyknotic nuclei. Both features are a consequence of apoptosis affecting neuroepithelial cells, which were in S-phase or shortly after. In addition, when the E5 embryos were maintained in ovo after the application of [methyl-3H]thymidine, 70% of the apoptotic retinal cells were labelled, indicating the in vivo prevalence of cell death among actively proliferating neuroepithelial cells. Apoptotic cell death is thus temporally and spatially regulated during proliferative stages of retinal neurogenesis, and embryonic proinsulin is presumably an endogenous protective factor.

Animals↗

PubMed1984

A new cell surface relationship between neuroepithelial cells during rat neural tube development.

Electron microscopic examination of the developing neural tube in 11th to 13th day rat fetuses revealed a new cell surface relationship between differentiating neuroepithelial cells. Cytoplasmic projections possessing terminal dilations were observed extending from neuroepithelial cells through cytoplasmic furrows into large coated pits at the surface of adjacent cells. This cell-to-cell relationship provides a mechanism for the internalization of surface molecules and possibly even cytoplasmic constituents. Communication between donor and recipient cells mediated in this way suggests a route for the sharing of macromolecules, including cytoplasmic fragments, which could function as regulators in embryonic development and differentiation.

Animals↗

PubMed1988

Role of cell-cycle in regulating neuroepithelial cell shape during bending of the chick neural plate.

Neuroepithelial cells transform from spindle-shaped to wedge-shaped within the median and paired dorsolateral hinge points of the bending neural plate, but the mechanisms underlying these localized changes are unclear. This study was designed to evaluate further the hypothesis that localized "wedging" of neuroepithelial cells during bending involves basal cellular expansion resulting from alteration of the cell-cycle. Neurulating chick embryos were treated with tritiated thymidine, and transverse sections through the midbrain were examined autoradiographically. Parameters of the cell-cycle as well as nuclear position and size were assessed in the median hinge point, which contains predominantly wedge-shaped cells, and in adjacent lateral areas of the neural plate, which contain predominantly spindle-shaped cells. Both the DNA-synthetic phase and non-DNA synthetic portion of the cell-cycle were significantly longer in the median hinge point than in lateral neuroepithelial areas, some nuclei in both regions were located basally during these phases, and virtually all basal nuclei in the median hinge point were large. Additionally, the mitotic phase was significantly shorter in the median hinge point than in lateral areas. We present a model to explain how alteration of the cell-cycle in the median hinge point could generate wedging of cells in this region.

Animals↗

PubMed2006

Etoposide induces apoptosis and cell cycle arrest of neuroepithelial cells in a p53-related manner.

We clarified that etoposide (VP-16), a topoisomerase II inhibitor, induced apoptosis in the mouse fetal brain. Apoptotic mechanisms and cell cycle arrest in this system were investigated. Four mg/kg of VP-16 was injected into pregnant mice on day 12 of gestation (GD12). The cell cycle and expression of protein and mRNA of p53 and its transcriptional target genes were examined in the fetal brain. The number of p53- and p21-protein-positive cells peaked at 4 h after treatment (HAT). The expression of p21 mRNA was significantly increased at 4 HAT and 8 HAT. The expression of fas mRNA was significantly increased from 2 to 12 HAT. Significant expression of puma mRNA was observed from 1 HAT to 48 HAT. Flow cytometric analysis revealed that VP-16 induced S-phase accumulation and G2 arrest at 4 and 8 HAT, and VP-16-induced apoptosis was significantly increased from 4 to 24 HAT. In an experiment using BrdU treatment of pregnant mice, the migration of neuroepithelial cells in the fetuses was delayed as compared to the migration of controls, and BrdU-positive signals were observed in some pyknotic cells from 8 to 12 HAT. The present results suggest that VP-16 might induce cell cycle arrest at G2/M phase and apoptosis in a p53-related manner.

Animals↗

PubMed2003

Direct binding of cell polarity protein PAR-3 to cell-cell adhesion molecule nectin at neuroepithelial cells of developing mouse.

PAR-3 is a cell polarity protein that localizes at tight junctions (TJs) by direct binding to an immunoglobulin (Ig)-like cell-cell adhesion molecule JAM-1 in mammalian epithelial cells. Another Ig-like cell-cell adhesion molecule nectin plays a role in the localization of JAM-1 at TJs in epithelial cells. Nectin furthermore plays a role in the organization of adherens junctions (AJs) and TJs. Nectin comprises a family of four members, nectin-1, -2, -3, and -4. Nectins are associated with the actin cytoskeleton through afadin, of which the PDZ domain binds to nectins through their C-terminal four amino acids. We show here that PAR-3 binds to nectin-1 and -3 in neuroepithelial cells of the embryonic telencephalon, which are equipped with AJs, but not with typical TJs. Nectin-1, -2, -3, and afadin, but not JAM-1, were concentrated at AJs in neuroepithelial cells of the embryonic telencephalon at E13.5 and PAR-3 co-localized with nectins. PAR-3 was co-immunoprecipitated with nectin-1 and -3, but not with nectin-2 or JAM-1, from the mouse whole brain at E13.5. Recombinant PAR-3 stoichiometrically bound to recombinant nectin-1 and -3. The first one of the three PDZ domains of PAR-3 bound to the C-terminal four amino acids of nectin-1 and -3. The affinities of PAR-3 and afadin for nectin-1 and -3 were similar. Cadherin-deficient L cells expressing nectin-1 and -3 formed nectin-1- and -3-based cell-cell junctions, respectively, where PAR-3 as well as afadin was recruited. These results indicate that nectin-1 and -3 are involved in the localization of PAR-3 at AJs in the neuroepithelial cells of the embryonic telencephalon.

Adaptor Proteins, Signal Transducing↗

PubMed1998

The effects of laminin on the characteristics and differentiation of neuronal cells from epidermal growth factor-responsive neuroepithelial cells.

Many extracellular matrix molecules are expressed in the embryonic nervous system and there is some evidence that they are important regulators of neural development. Of these molecules, laminin appears to be the most potent, affecting virtually all neurons of the peripheral and central nervous system. This study was undertaken to investigate the effects of laminin on the proliferation and differentiation of cultured neuroepithelial cells taken from fetal rat forebrains (embryonic day 17-19). The results are summarized as follows. 1) Neuroepithelial cells cultivated in epidermal growth factors containing serum-free medium subsequently differentiated into neurons, astrocytes, and oligodendrocytes. 2) Neuronal cells derived from neuroepithelial cells were immunoreactive for gamma-aminobutyric acid (GABA) or substance P, but were not for serotonin and tyrosine hydroxylase. 3) In western blot analysis, the phosphorylated neurofilament content in neuronal cells was higher in culture on laminin than in culture on poly-L-lysine (PLL). 4) The proliferation rate of GABAergic neurons was higher in culture on laminin than in culture on PLL. These results suggest that GABAergic and substance P-ergic neurons can be differentiated from neuroepithelial cells and that laminin promotes the differentiation of neuronal cells from neuroepithelial cells and the increased proliferation rate of GABAergic cells.

Animals↗

PubMed1977

Brain-associated cell surface antigens on neuroepithelial cells in a transplantable mouse teratoma.

Mouse neonatal brain cell fractions enriched for surface membranes were used as immunogens to produce a heterologous immune serum. Following absorption to remove non-neural anti-mouse activity, this serum demonstrated by microcomplement fixation an anti-brain activity that was completely removed by absorption with neonatal mouse brain or with solid tumors of the mouse transplantable teratoma OTT-6050. Indirect immunofluorescence applied to living monolayer cultures of differentiating teratoma embryoid bodies showed the absorbed serum's reaction with neural cell surfaces only. In material studied with frozen sections, the absorbed serum recognized antigenic sites in all examined areas of both neonatal and adult mouse brain, and only within neuroepithelial cell populations of solid transplants of the teratoma.

Animals↗

PubMed2003

An inhibition of cyclin-dependent kinases that lengthens, but does not arrest, neuroepithelial cell cycle induces premature neurogenesis.

The G1 phase of the cell cycle of neuroepithelial cells, the progenitors of all neurons of the mammalian central nervous system, has been known to lengthen concomitantly with the onset and progression of neurogenesis. We have investigated whether lengthening of the G1 phase of the neuroepithelial cell cycle is a cause, rather than a consequence, of neurogenesis. As an experimental system, we used whole mouse embryo culture, which was found to exactly reproduce the temporal and spatial gradients of the onset of neurogenesis occurring in utero. Olomoucine, a cell-permeable, highly specific inhibitor of cyclin-dependent kinases and G1 progression, was found to significantly lengthen, but not arrest, the cell cycle of neuroepithelial cells when used at 80 microM. This olomoucine treatment induced, in the telencephalic neuroepithelium of embryonic day 9.5 to 10.5 mouse embryos developing in whole embryo culture to embryonic day 10.5, (i) the premature up-regulation of TIS21, a marker identifying neuroepithelial cells that have switched from proliferative to neuron-generating divisions, and (ii) the premature generation of neurons. Our data indicate that lengthening G1 can alone be sufficient to induce neuroepithelial cell differentiation. We propose a model that links the effects of cell fate determinants and asymmetric cell division to the length of the cell cycle.

Animals↗

PubMed1996

Effects of FGF-1 and FGF-2 on GD3 immunoreactive spinal neuroepithelial cells.

Embryonic central nervous system neuroepithelial cells are a transient population of cells that give rise to neuronal and glial progenitors. In the E12-E16 embryonic rat spinal neural tube we have identified neuroepithelial cells as radially oriented cells expressing the GD3 ganglioside as recognized by the monoclonal anti-GD3 ganglioside antibodies, R24 and LB1. In vitro, neuroepithelial cells, which migrate from the ventral aspect of E12 rat lumbosacral neural tube explants, also express GD3 ganglioside immunoreactivity, thus permitting their distinction from neural crest cells (NCC) which migrate from the dorsal aspect of such explants. Fibroblast growth factor-1 (FGF-1, acidic FGF) and FGF-2 (basic FGF) increase the migration of neuroepithelial cells and the extent to which they incorporate the thymidine analogue bromodeoxyuridine (BrdU). They do not, however, alter the rate at which these migrating neuroepithelial cells undergo cell death. Previous observations established the actions of FGF-1 and FGF-2 on neuronal and glial cells. The present study indicates that these growth factors also influence the motility and proliferation of progenitor cells at a developmental stage which precedes their divergence into neuronal and glial lineages.

Animals↗

PubMed1994

A short term analysis of the behaviour of conditionally immortalized neuronal progenitors and primary neuroepithelial cells implanted into the fetal rat brain.

Conditionally immortalized (temperature-sensitive) striatal-derived neuronal progenitor cell lines and primary neuroepithelial cells were transplanted into the CNS of gestational day 15-16 rat fetuses using an 'in utero' surgical procedure. Each fetus received 2.5-3 x 10(4) donor cells previously labelled in vitro by incubation with 5-bromo-2'-deoxyuridine (BrdU). At 5 days following transplantation, 69% of the fetuses were still alive. Engrafted cells were detected by BrdU immunohistochemistry, and the appearance of the engrafted cells and the time course of Nestin and PCNA expression were measured at 6, 24, 64 h and 5 days after transplantation. The evolution of Large T-Antigen immunoreactivity in engrafted temperature-sensitive (ts) cells was also evaluated at the above time intervals. The results indicate that the majority of the implanted cells were aggregated into clusters 24 h after transplantation. These clusters were not visible at 6 h, when most of the cells were isolated. The clusters were located in both the ventricles and parenchyma. These findings were common to both ts cells and striatal primary neuroepithelial cells. At 64 h and 5 days, isolated cells associated with the germinal layer and scattered throughout the parenchyma were also found. In the clusters, Nestin expression decreased proportionally with time following transplantation. Furthermore, Large T-Antigen immunoreactivity disappeared from ts cells between 6 and 24 h after transplantation. Finally, measurements of the temporal evolution of PCNA expression within the clusters indicate a progressive reduction in the mitotic activity of the transplanted cells. The results demonstrate that striatal primary neuroepithelial cells and conditionally immortalized neuronal progenitors can survive, migrate and/or compartimentalize into clusters whilst changing their antigenic properties and ability to proliferate.

Animals↗

PubMed1995

Late-migrating neuroepithelial cells from the spinal cord differentiate into sensory ganglion cells and melanocytes.

During embryonic development, neural crest cells give rise to many structures in peripheral tissues. Other neural tube cells are thought to contribute only to structures within the CNS. In contrast to this idea, we report a second wave of migration of cells away from the spinal cord occurring after the emigration of crest cells is complete. Neuroepithelial cells from spinal cords in E5 chicken embryos migrate into the periphery and differentiate into neurons and satellite cells within sensory ganglia and into melanocytes in skin and feathers. These results show that some cell types previously considered to be the descendants exclusively of neural crest cells are also derived from neuroepithelial cells in the spinal cord.

Animals↗

PubMed2003

Retinal ganglion cell-derived sonic hedgehog signaling is required for optic disc and stalk neuroepithelial cell development.

The development of optic stalk neuroepithelial cells depends on Hedgehog (Hh) signaling, yet the source(s) of Hh protein in the optic stalk is unknown. We provide genetic evidence that sonic hedgehog (Shh) from retinal ganglion cells (RGCs) promotes the development of optic disc and stalk neuroepithelial cells. We demonstrate that RGCs express Shh soon after differentiation, and cells at the optic disc in close proximity to the Shh-expressing RGCs upregulate Hh target genes, which suggests they are responding to RGC-derived Shh signaling. Conditional ablation of Shh in RGCs caused a complete loss of optic disc astrocyte precursor cells, resulting in defective axon guidance in the retina, as well as conversion of the neuroepithelial cells in the optic stalk to pigmented cells. We further show that Shh signaling modulates the size of the Pax2(+) astrocyte precursor cell population at the optic disc in vitro. Together, these data provide a novel insight into the source of Hh that promotes neuroepithelial cell development in the mammalian optic disc and stalk.

Animals↗

PubMed2001

Direct cell-cell interactions control apoptosis and oligodendrocyte marker expression of neuroepithelial cells.

During brain development, the neuroepithelium generates neurons and glial cells. Proliferation and differentiation of neuroepithelial cells are controlled by a complex combination of secreted factors and more intrinsic or local mechanisms, such as lateral inhibition and asymmetric division. To obtain further insights into the signals governing neuroepithelial cell fate, we used the immortomouse to derive conditionally immortalised cell lines from mouse E10 neuroepithelium. We isolated a nestin-positive basic fibroblast growth factor (bFGF)-responsive cell line (SVE10-23) which mostly differentiate into astrocytes when cocultured with primary cortical cells. We found that, by simply lowering the cell density, SVE10-23 cells embarked on oligodendrocytic differentiation as indicated by the strong expression of galactocerebroside C and 2'3'-cyclic nucleotide 3'-phosphodiesterase. Apoptosis accompanied the differentiation, and all cells died within 1 week. We present here evidence that direct interactions between cells are the main mechanism regulating this oligodendrocytic differentiation. We demonstrate that SVE10-23 cells contact or proximity inhibit their differentiation, prevent apoptosis, and promote their proliferation. Similarly, others nestin-positive precursor cell lines and nonimmortalised bFGF-grown E10 cells were found to spontaneously differentiate at low density, thus generalising the idea that neural precursor fate is regulated by direct cell-cell interactions. The SVE10-23 cell line provides a valuable tool with which to study further the molecular components implicated in this mode of regulation.

2',3'-Cyclic Nucleotide 3'-Phosphodiesterase↗