Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Neural cells”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed2004

Human adult craniofacial muscle-derived cells: neural-cell adhesion-molecule (NCAM; CD56)-expressing cells appear to contain multipotential stem cells.

Skeletal muscle has been well characterized as a reservoir of myogenic precursors or satellite cells with the potential to participate in cellular repopulation therapies for muscle dysfunction. Recent evidence, however, suggests that the postnatal muscle compartment can be considered an alternative to bone marrow as a source of multipotent cells or muscle-derived stem cells (MDSCs). MDSCs, when primed with appropriate environmental cues, can differentiate into a variety of non-muscle cells. The present study describes the application of a new technique for the isolation of adult human myoblasts and putative MDSCs, based on microbead-immunomagnetic selection of CD56+ cells, derived from craniofacial skeletal muscle, and details changes in morphological/molecular phenotype of the purified cells when maintained in either a myogenic or a non-myogenic milieu. Multiple immunofluorescence microscopy and two-colour flow-cytometric analysis of proliferating CD56+ cultures revealed positive staining for myogenic markers (CD56, desmin and M-cadherin) as well as putative stem-cell markers [the antigens CD34, CD90 and CD106, and Flk-1 (fetal liver kinase-1)/VEGFR-2 (vascular-endothelial-growth-factor receptor)]. Confluent cultures subjected to cycles of adipogenic or osteogenic induction contained either adipocytes or osteoblasts and myotubes. In conclusion, the CD56+ subpopulation within adult human skeletal muscle is heterogeneous and is composed of both lineage-committed myogenic cells and multipotent cells (the candidate MDSCs), which are able to form non-muscle tissue such as fat and bone.

Adipocytes↗
PubMed1994

[The expression of neural cell adhesion molecule (NCAM), neural invasion and recurrence patterns in rectal cancer--a study using anti-NACM (neural cell adhesion molecule) antibody].

Neural invasion may be one of the main causes of local recurrence, but its mechanism has not been sufficiently clarified. We previously reported that the expression of NCAM on cancer cells was correlated with neural invasion in pancreatic cancer. In this study, we examined the neural affinity of rectal cancer cells and the relationship between neural invasion and recurrence patterns of rectal cancers. A total of 64 rectal adenocarcinoma were examined. Specimens from 17 patients (27%) revealed perineural invasion. The incidence of neural invasion increased with the frequency of venous invasion and the degree of lymph node metastasis, but not significantly. The incidence of the expression of NCAM in rectal cancer cell was 45.3 percent. Neural invasion of rectal carcinoma was significantly related to the expression of NCAM (p < 0.05). NCAM immunocytolocalization was classified into the focal type, and the diffuse type. Concerning the recurrence type, 8 of 9 cases that developed local recurrence showed either presence of neural invasion or expression of NCAM. Liver metastasis was associated with absence of neural invasion or NCAM expression. The expression of NCAM may contribute to local recurrence, whereas the absence of NCAM may predict liver metastasis.

Adenocarcinoma↗
PubMed2003

Neural cell adhesion molecule (NCAM) association with PKCbeta2 via betaI spectrin is implicated in NCAM-mediated neurite outgrowth.

In hippocampal neurons and transfected CHO cells, neural cell adhesion molecule (NCAM) 120, NCAM140, and NCAM180 form Triton X-100-insoluble complexes with betaI spectrin. Heteromeric spectrin (alphaIbetaI) binds to the intracellular domain of NCAM180, and isolated spectrin subunits bind to both NCAM180 and NCAM140, as does the betaI spectrin fragment encompassing second and third spectrin repeats (betaI2-3). In NCAM120-transfected cells, betaI spectrin is detectable predominantly in lipid rafts. Treatment of cells with methyl-beta-cyclodextrin disrupts the NCAM120-spectrin complex, implicating lipid rafts as a platform linking NCAM120 and spectrin. NCAM140/NCAM180-betaI spectrin complexes do not depend on raft integrity and are located both in rafts and raft-free membrane domains. PKCbeta2 forms detergent-insoluble complexes with NCAM140/NCAM180 and spectrin. Activation of NCAM enhances the formation of NCAM140/NCAM180-spectrin-PKCbeta2 complexes and results in their redistribution to lipid rafts. The complex is disrupted by the expression of dominant-negative betaI2-3, which impairs binding of spectrin to NCAM, implicating spectrin as the bridge between PKCbeta2 and NCAM140 or NCAM180. Redistribution of PKCbeta2 to NCAM-spectrin complexes is also blocked by a specific fibroblast growth factor receptor inhibitor. Furthermore, transfection with betaI2-3 inhibits NCAM-induced neurite outgrowth, showing that formation of the NCAM-spectrin-PKCbeta2 complex is necessary for NCAM-mediated neurite outgrowth.

Animals↗
PubMed2001

Expression of neural cell adhesion molecules (polysialylated form of neural cell adhesion molecule and L1-cell adhesion molecule) on resected small cell lung cancer specimens: in relation to proliferation state.

BACKGROUND AND OBJECTIVES: Alteration of homotypic cell-cell adhesion has been suggested to play an important role in tumor progression. The present study examined the relationship between neural cell adhesion molecules and state of proliferation of small cell lung cancer (SCLC) cells. METHODS: Seventeen surgically resected specimens of SCLC were immunohistochemically examined, by using monoclonal antibodies against neural cell adhesion molecule (NCAM) and its polysialic acid side chains, and L1 cell adhesion molecule (L1-CAM). Ki-67 labeling indices were also determined immunohistochemically. RESULTS: All patients were positive for L1-CAM. Fifteen patients (88.2%) were positive for NCAM. Among the fifteen patients, nine (60.0%) were positive for NCAM PSA side chain. The probability of survival of the NCAM without PSA side chain group was significantly higher than that of the NCAM with PSA side chain group (log-rank test; P = 0.500). CONCLUSIONS: The expression of NCAM with PSA side chains might be a prognostic factor and NCAM a marker for SCLC. L1-CAM may be synthesized independent of state of proliferation of individual tumor cell and may affect clinical feature of SCLC.

Adolescent↗
PubMed2006

Dynamic changes of gangliosides expression during the differentiation of embryonic and mesenchymal stem cells into neural cells.

Stem cells are used for the investigation of developmental processes at both cellular and organism levels and offer tremendous potentials for clinical applications as an unlimited source for transplantation. Gangliosides, sialic acid-conjugated glycosphingolipids, play important regulatory roles in cell proliferation and differentiation. However, their expression patterns in stem cells and during neuronal differentiation are not known. Here, we investigated expression of gangliosides during the growth of mouse embryonic stem cells (mESCs), mesenchymal stem cells (MSCs) and differentiated neuronal cells by using high-performance thin-layer chromatography (HPTLC). Monosialoganglioside 1 (GM1) was expressed in mESCs and MSCs, while GM3 and GD3 were expressed in embryonic bodies. In the 9-day old differentiated neuronal cells from mESCs cells and MSCs, GM1 and GT1b were expressed. Results from immunostaining were consistent with those observed by HPTLC assay. These suggest that gangliosides are specifically expressed according to differentiation of mESCs and MSCs into neuronal cells and expressional difference of gangliosides may be a useful marker to identify differentiation of mESCs and MSCs into neuronal cells.

Animals↗
PubMed2002

Adult T-cell leukemia (ATL) cells which express neural cell adhesion molecule (NCAM) and infiltrate into the central nervous system.

We encountered a patient with adult T-cell leukemia/lymphoma (ATL) which expressed neural cell adhesion molecule (NCAM). The tumor cells markedly infiltrated the central nervous system (CNS) during the course of the ATL. The patient died 20 months after disease onset, which was considered to be early in the course. During the invasion of the CNS, the surface phenotype of the peripheral blood ATL cells by flow cytometric analysis was CD2+, CD3+, CD4+, CD7-, CD8-, CD16-, NCAM (CD56)+, HLA-DR-. We speculate that the infiltration of ATL cells into the CNS was closely related to the expression of the NCAM in this patient.

Blotting, Southern↗
PubMed1999

Neuronal progenitor-like cells expressing polysialylated neural cell adhesion molecule are present on the ventricular surface of the adult rat brain and spinal cord.

In the adult rodent brain, it is now well established that neurons are continuously generated from proliferating neuronal progenitor cells located in the subventricular zone of the lateral ventricle (SVZ) and the dentate gyrus of the hippocampus. Recently, it has been shown that neurons can also be generated in vitro from various regions of the adult brain and spinal cord ventricular neuroaxis. As the highly polysialylated neural cell adhesion molecule (PSA-NCAM) has been shown to be specifically expressed by neuronal progenitor cells of the SVZ and the hippocampus, the present study was designed to determine whether cells expressing this molecule could be detected in the vicinity of the ventricular system of the adult rat brain and spinal cord. After double or triple immunostaining for different neuronal and glial markers, confocal microscopy was used to examine the surface of the ventricular neuroaxis in either 40- to 50-microm-thick transverse vibratome sections cut through different brain regions, or in 200- to 300-microm-thick tissue slices including the intact surface of the brain ventricles or of the spinal cord central canal. In untreated rats, PSA-NCAM, microtubule associated protein 2 (MAP2) and class III-beta-tubulin were found to be associated with a number of neuron-like cells located on the surface of the third and fourth ventricles and of the spinal cord central canal. The proliferation of the PSA-NCAM-immunoreactive (IR) neuron-like cells detected on the surface of the third and fourth ventricles was not affected by injection of epidermal growth factor (EGF) or basic fibroblast growth factor (bFGF) into these ventricles, but was stimulated by the combined injection of EGF + bFGF. These data indicate that cells exhibiting features of neuronal progenitors are present on the ependymal surface of the adult rat brain and spinal cord ventricular axis.

Age Factors↗
PubMed1996

Human first-trimester placenta intra-arterial trophoblast cells express the neural cell adhesion molecule.

The supposed influence of endometrial natural killer (NK) cells on the trophoblast invasion activities especially on intravasation of uteroplacental arteries in the non-pathogenic human first-trimester placenta was studied by means of immunohistochemistry. To identify extravillous trophoblast cells, smooth muscle cells, endothelia, endometrial glands, decidual stroma cells and endometrial NK cells, antibodies against cytokeratins, vimentin, smooth muscle cells, epithelium specific antigen and endothelial cells were employed. Furthermore, the immunohistochemical distribution patterns of CD56, CD57 and CD94 were studied and compared with the localization of invading trophoblast cells. Remodelling and dilatation of uteroplacental arteries starts before trophoblast cells can be found in the vicinity of the vessels. Nevertheless, subsequent trophoblast invasion of the arterial wall will lead to media destruction and intravasation only on focally restricted areas. This process is accompanied by the disappearance of endothelial cells and the immediate expression of the neural cell adhesion molecule (N-CAM, CD56) by intra-arterial trophoblast cells, which are eventually beginning to form intraluminal plugs. These findings led us to the conclusion that in the human pregnancy-induced physiological changes of the uteroplacental blood flow and the peripheral blood NK cell activity is not only, but also, due to the effect of CD56 expression by intra-arterial trophoblast cells.

Antibodies, Monoclonal↗
PubMed1993

Osteogenic protein-1 regulates L1 and neural cell adhesion molecule gene expression in neural cells.

Osteogenic protein-1 (OP-1) is a member of the TGF-beta superfamily that is expressed in the nervous system. We recently showed that human recombinant osteogenic protein-1 (hOP-1) strongly promotes the aggregation of dividing neuroblastoma x glioma hybrid NG108-15 cells, in part by inducing the major isoforms of the neural cell adhesion molecule (N-CAM) (Perides, G., Safran, R. M., Rueger, D. C., and Charness, M. E. (1992) Proc. Natl. Acad. Sci. U. S. A. 89, 10326-10330). Here we show that hOP-1 induces L1 expression approximately 6-fold in NG108-15 cells without changing the levels of N-cadherin, neurofilament 200, Thy-1, tau, and G alpha s. OP-1 induction of L1 and N-CAM was unassociated with changes in cell proliferation and was not reproduced by cellular differentiation. The increased adhesiveness of hOP-1-treated NG108-15 cells could be inhibited in part by Fab fragments of an anti-L1 polyclonal antiserum. L1 and N-CAM expression first increased 12-18 h after hOP-1 treatment, reached a maximum after 2-3 days, persisted for up to 5 days, and returned to control levels 3 days after hOP-1 withdrawal. The increases in L1 and N-CAM protein levels were preceded or accompanied by large increases in the abundance of L1 and all detectable N-CAM mRNAs. Actinomycin D prevented the induction by hOP-1 of L1 and N-CAM mRNAs, suggesting that hOP-1 regulates immunoglobulin CAM gene transcription. OP-1 is the first described growth factor that regulates both N-CAM and L1 gene expression.

Bone Morphogenetic Protein 7↗
PubMed1996

Conditionally Immortalized Neural Cell Lines: Potential Models for the Study of Neural Cell Function

Studies on primary cell cultures have contributed significantly to our understanding of neural cell function. Nevertheless, for many studies the value of these primary cell cultures has been limited by the time the cultures survive in vitro, the quantity of cellular material available for analysis, and the need to prepare the cells on a regular basis from fresh tissue. Techniques for immortalizing cells have existed for some time, but the repertoire of immortalizing genes has grown significantly. This has expanded our ability to generate useful cell lines of specific neural types that are better models of the in vivo phenotype than previously. The constitutive expression of oncogenes keeps cells in a proliferative state that could lead to the loss of differentiated gene expression and function. An appealing improvement of immortalization methodology is the use of temperature-sensitive oncogenes that generate cell lines that can proliferate at a permissive temperature and "differentiate" at a nonpermissive temperature. The proliferation of such conditionally immortalized cell lines can be suppressed simply by increasing the temperature. Cell lines maintained at the nonpermissive temperature can enter into a stage in which they express differentiated properties of the cell. The potential ability of conditionally immortalized neural cell lines to accurately reflect their in vivo function has now been demonstrated on several occasions through transplantation experiments. In this report, the generation of these cell lines is described along with a discussion of their potential applications in neurobiology.

Journal Article↗
PubMed2002

Neural cell adhesion molecule (NCAM) promotes the differentiation of hippocampal precursor cells to a neuronal lineage, especially to a glutamatergic neural cell type.

Rat hippocampal precursor cells isolated from hippocampi of embryonic day 16.5 (E16.5) rat embryos were found to proliferate in the presence of basic fibroblast growth factor. Addition of soluble neural cell adhesion molecule (NCAM) to these precursor cells reduced cell proliferation in a dose dependent manner and enhanced the induction of precursor cells' differentiation to the neuronal lineage. Given these findings that NCAM induces the differentiation of hippocampal precursor cells, we investigated possible effects of NCAM on the expression of basic helix-loop-helix (bHLH) transcription factors during the differentiation. Soluble NCAM upregulated the transcription of bHLH transcription factors, neurogenin1 and NeuroD, but decreased HES5. Western blot analysis showed that NCAM increased the expression levels of CaMKII, p-MAPK, GluR1 and NR1 but decreased p-STAT3. These results support a role for NCAM in the inhibition of proliferation and the induction of neural differentiation of hippocampal neural precursor cells, and act as developmental regulators of the bHLH families, ultimately leading to the generation of glutamatergic neural cell types in the differentiation of hippocampal precursor cells.

Animals↗
PubMed1994

Investigation of karyotypic, morphologic and clinical features in patients with acute myeloid leukemia blast cells expressing the neural cell adhesion molecule (CD56).

The mechanisms of extramedullary leukemic infiltration are not well characterized. The cell-surface glycoprotein CD56, which is identical to the neural cell adhesion molecule, may be involved. Using the Leu-19 antibody and flow cytometric methods, the leukemic blasts of 22% (70 of 314) of patients were CD56 positive. This was most common in acute monocytic leukemia (15 of 18, 83%) and in patients with the cytogenetic abnormalities t(8;21) (seven of 13, 54%) and trisomy 8 (nine of 22, 41%). CD56 expression was not associated with extramedullary leukemic infiltration, but was correlated with positivity for CD11b (p < 0.001), CD14 (p < 0.001) and CD19 (p = 0.018). Although associated with morphologic and cytogenetic features, CD56 expression alone cannot account for most instances of tissue infiltration in acute myeloid leukemia (AML).

Adolescent↗
PubMed2000

Adult bone marrow stromal cells differentiate into neural cells in vitro.

Bone marrow stromal cells (BMSC) normally give rise to bone, cartilage, and mesenchymal cells. Recently, bone marrow cells have been shown to have the capacity to differentiate into myocytes, hepatocytes, and glial cells. We now demonstrate that human and mouse BMSC can be induced to differentiate into neural cells under experimental cell culture conditions. BMSC cultured in the presence of EGF or BDNF expressed the protein and mRNA for nestin, a marker of neural precursors. These cultures also expressed glial fibrillary acidic protein (GFAP) and neuron-specific nuclear protein (NeuN). When labeled human or mouse BMSC were cultured with rat fetal mesencephalic or striatal cells, a small proportion of BMSC-derived cells differentiated into neuron-like cells expressing NeuN and glial cells expressing GFAP.

Animals↗
PubMed1995

Neural cells from dogfish embryos express the same subtype-specific antigens as mammalian neural cells in vivo and in vitro.

Neural cells are classically identified in vivo and in vitro by a combination of morphological and immunocytochemical criteria. Here, we demonstrate that antibodies used to identify mammalian oligodendrocytes, neurons, and astrocytes recognize these cell types in the developing spiny dogfish central nervous system and in cultures prepared from this tissue. Oligodendrocyte-lineage-specific antibodies O1, O4, and R-mAb labeled cells in the 9 cm dogfish brain stem's medial longitudinal fascicle (MLF) and in areas lateral to it. Process-bearing cells, cultured from the dogfish brain stem, were also labeled with these antibodies. An anti-lamprey neurofilament antibody (LCM), which recognized 60 and 150 kDa proteins in dogfish brain stem homogenates, labeled axons and neurons in the brain stem and axons in the cerebellum of the dogfish embryo. It also labeled cell bodies and/or processes of some cultured cerebellar cells. An anti-bovine glial fibrillary acidic protein antibody, which recognized 42-44 kDa protein(s) in dogfish brain stem homogenates, labeled astrocyte-like processes in the brain stem and cerebellum of the dogfish embryo and numerous large and small flat cells in the cerebellar cultures. These results demonstrate that dogfish oligodendrocytes, neurons, and astrocytes express antigens that are conserved in mammalian neural cells. The ability to culture and identify neural cell types from cartilaginous fish sets the stage for studies to determine if proliferation, migration, and differentiation of these cell types are regulated in a similar fashion to mammalian cells.

Animals↗
PubMed1992

BEN, a novel surface molecule of the immunoglobulin superfamily on avian hemopoietic progenitor cells shared with neural cells.

BEN is a novel molecule of the immunoglobulin superfamily that we previously identified by means of a monoclonal antibody on neural cell populations during avian development and epithelial cells of the bursa of Fabricius. In this paper, we describe the expression of BEN by hemopoietic cells during ontogeny. In the thymus, BEN is expressed as early as E9, and from E12 until just after hatching 30-60% of thymocytes are BEN positive. Thus the cells expressing BEN are immature thymocytes and not yet differentiated T cells. In the spleen, BEN expression parallels the myelopoietic activity. It is present on 75% of splenocytes during embryonic development and falls rapidly to 20% of cells during the first week after hatching when the spleen is becoming a secondary lymphoid organ. BEN is also found on a large proportion (about 80% positive cells) of bone marrow cells during ontogeny. Post hatching, BEN is present on 40-50% of bone marrow cells. The population of BEN-positive cells in the bone marrow includes myeloid and erythroid progenitor cells, identified by their ability to form colonies in vitro. BEN expression is lost as progenitor cells proliferate and differentiate to develop mature colonies in the clonal assay. Mature myeloid cells, such as macrophages, granulocytes, thrombocytes, and erythrocytes do not express the BEN antigen. Taken together, these data demonstrated that BEN is a stage-specific rather than a lineage-specific differentiation antigen expressed by immature hemopoietic cells.

Activated-Leukocyte Cell Adhesion Molecule↗
PubMed2006

Permanent, sex-selective effects of prenatal or adolescent nicotine exposure, separately or sequentially, in rat brain regions: indices of cholinergic and serotonergic synaptic function, cell signaling, and neural cell number and size at 6 months of age.

Nicotine is a neuroteratogen that disrupts neurodevelopment and synaptic function, with vulnerability extending into adolescence. We assessed the permanence of effects in rats on indices of neural cell number and size, and on acetylcholine and serotonin (5HT) systems, conducting assessments at 6 months of age, after prenatal nicotine exposure, adolescent exposure, or sequential exposure in both periods. For prenatal nicotine, indices of cell number and size showed few abnormalities by 6 months, but there were persistent deficits in cerebrocortical choline acetyltransferase activity and hemicholinium-3 binding to the presynaptic choline transporter, a pattern consistent with cholinergic hypoactivity; these effects were more prominent in males than females. The expression of 5HT receptors also showed permanent effects in males, with suppression of the 5HT(1A) subtype and upregulation of 5HT(2) receptors. In addition, cell signaling through adenylyl cyclase showed heterologous uncoupling of neurotransmitter responses. Nicotine exposure in adolescence produced lasting effects that were similar to those of prenatal nicotine. However, when animals were exposed to prenatal nicotine and received nicotine subsequently in adolescence, the adverse effects then extended to females, whereas the net effect in males was similar to that of prenatal nicotine by itself. Our results indicate that prenatal or adolescent nicotine exposure evoke permanent changes in synaptic function that transcend the recovery of less-sensitive indices of structural damage; further, prenatal exposure sensitizes females to the subsequent adverse effects of adolescent nicotine, thus creating a population that may be especially vulnerable to the lasting behavioral consequences of nicotine intake in adolescence.

Acetylcholine↗
PubMed1991

Double screening of suramin derivatives on human colon cancer cells and on neural cells provides new therapeutic agents with reduced toxicity.

Suramin is a polyanionic compound currently used under evaluation for antineoplastic activity. One of the main problems encountered during clinical trials was an adverse neurotoxic effect, probably due to a direct cytotoxic effect on neural cells. Suramin is also known to trigger differentiation of human colon cancer cells, yet a chronic treatment induces a lysosomal storage disorder. The aim of this study was to evaluate suramin analogs for their effect: (i) on the lysosomal system of the human colon cancer cell clone HT29-D4; and (ii) on C6 glioma cell growth and morphology. One of the derivatives tested, NF036, induced terminal differentiation of HT29-D4 cells without any impairment of the lysosomal system. Furthermore, in contrast to suramin, NF036 did not alter C6 cell growth and morphology. We conclude that there is a relationship between the ability of a suramin derivative to induce a lysosomal storage disorder in human colon cancer cells and its neurotoxic effect. A double screening of suramin analogs on HT29-D4 and C6 cells allowed us to identify a new candidate antineoplastic drug: NF036.

Antineoplastic Agents↗
PubMed2005

XNGNR1-dependent neurogenesis mediates early neural cell death.

Early neural cell death is programmed cell death occurring within proliferating and undifferentiated neural progenitors. Little is known about the regulation and role of early neural cell death. In Xenopus embryos, primary neurogenesis is disrupted following the inhibition of early neural cell death, indicating that it is required for normal primary neurogenesis. Here we show that early neural cell death is dependent on primary neurogenesis. Overexpression of XSoxD concomitantly reduced N-Tubulin expression and early neural cell death, as seen by reduced TUNEL staining in stage 15 embryos. Conversely, overexpression of XNgnr1 led to ectopic N-Tubulin expression and TUNEL staining. However, XNeuroD overexpression, which induces ectopic N-Tubulin expression downstream of XNgnr1, had no effect on early neural cell death. E1A12S differentially inhibits the differentiation pathway induced by XNGNR1 protein. E1A12S-mediated inhibition of XNGNR1 neurogenic activity resulted in the reduction of N-Tubulin expression and TUNEL staining. Taken together, our data establish that primary neurogenesis induced by XNGNR1 promotes early neural cell death. This indicates that XNgnr1 positively regulates early neural cell death. We propose that early neural cell death might eliminate cells with abnormally high levels of XNGNR1, which can result in pre-mature neuronal differentiation.

Animals↗