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PubMed2001

Mutation in the neural cell adhesion molecule interferes with the differentiation of anterior pituitary secretory cells.

The neural cell adhesion molecule (NCAM) and its polysialylated isoform (PSA-NCAM) have been shown to influence the proliferation, differentiation and survival of different cell types. Here, we report the pattern of expression of NCAM and PSA-NCAM in the anterior lobe (AL) of the pituitary gland of the adult mouse. We demonstrate that the majority of cells express NCAM, while PSA-NCAM is retained mostly on corticotropes. Analysis of bromodeoxyuridine (BrdU) incorporation shows that the presence of PSA-NCAM on corticotropes is not related to proliferation but most likely to their functional properties. We subsequently analyzed defects induced by NCAM deficiency in adult NCAM knockout mice. In these mice, all secretory cell types in the AL are present and their distribution within the gland is similar to that in wild-type mice. However, proliferation of AL cells is significantly increased. In particular, more BrdU-positive cells are detected among somatotropes and mammotropes in NCAM-deficient mice. In addition, the percentages of secretory cells are changed: somatotropes are more numerous while the number of corticotropes is reduced. These data demonstrate the involvement of NCAM in the proper generation and/or maintenance of the different cell populations in the AL and suggest the importance of PSA in corticotrope functioning.

Animals↗
PubMed1989

Embryonic neural cell adhesion molecules on human natural killer cells.

The neural cell adhesion molecules (NCAM) are surface glycoproteins that were first described in brain tissue. NCAM mediate adhesion in a variety of cell-cell interactions. In the present study we show that the so-called "embryonic" NCAM, i.e., the highly polysialylated forms of these proteins, are expressed on natural killer cells and some CD3+ cells in man. Homotypic binding of NCAM, believed to be of importance for cell-cell adhesion in neural tissues, appears not to be essential for NK cell-mediated killing. Yet, NCAM might be involved in NK cell migration, homing or related functions.

Antibodies, Monoclonal↗
PubMed1992

Human immunodeficiency virus type 1-infected monocytic cells can destroy human neural cells after cell-to-cell adhesion.

Primary cultures of human embryonic neurons and astrocytes have been used to test the interactions between neural cells and either human immunodeficiency virus type 1 (HIV-1) or HIV-1-infected monocytes. After direct infection with HIV-1, neither morphological alteration of neurons and astrocytes nor signs of viral replication were observed. Similarly, cultured human neurons and astrocytes were resistant to incubation with the supernatant of HIV-1-infected U937 cells, a human monoblastoid cell line. In contrast, HIV-1-infected U937 monocytic cells adhered to neural cells and induced large plaques of necrosis surrounding them. This cytopathic effect began at the time of viral replication (day 16 after infection). Its intensity depended on that of viral replication, and its range was identical to the region of diffusion of viral antigens, as judged by immunocytochemistry. The cytopathic effect was not dependent on the release of free radicals. It could not be induced by cytokines or cytokine-stimulated U937 cells. It is likely that this cytopathic effect depends on the release of viral antigens either within the site of adherence itself or within close range of the astrocyte membrane.

Acquired Immunodeficiency Syndrome↗
PubMed2005

Quiescent neural cells regain multipotent stem cell characteristics influenced by adult neural stem cells in co-culture.

The source of cells participating in central nervous system (CNS) tissue repair and regeneration is poorly defined. One possible source is quiescent neural cells that can persist in CNS in the form of dormant progenitors or highly specialized cell types. Under appropriate conditions, these quiescent cells may be capable of re-entering the mitotic cell cycle and contributing to the stem cell pool. The aim of this study was to determine whether in vitro differentiated neural stem cells (NSC) can regain their multipotent-like stem cell characteristics in co-culture with NSC. To this end, we induced neural differentiation by plating NSC, derived from the periventricular subependymal zone (SEZ) of ROSA26 transgenic mice in Neurobasal A/B27 medium in the absence of bFGF. Under these conditions, NSC differentiated into neurons, glia, and oligodendrocytes. While the level of Nestin expression was downregulated, persistence of dormant progenitors could not be ruled out. However, further addition of bFGF or bFGF/EGF with conditioned medium derived from adult NSC did not induce any noticeable cell proliferation. In another experiment, differentiated neural cells were cultured with adult NSC, isolated from the hippocampus of Balb/c mice, in the presence bFGF. This resulted in proliferating colonies of ROSA26 derived cells that mimicked NSC in their morphology, growth kinetics, and expressed NSC marker proteins. The average nuclear area and DAPI fluorescence intensity of these cells were similar to that of NSC grown alone. We conclude that reactivation of quiescent neural cells can be initiated by NSC-associated short-range cues but not by cell fusion.

Animals↗
PubMed1979

Cell type-specific neural cell surface antigens.

Immunological methods have served to define several cell surface antigens that are differentially expressed among neural cell types and are developmentally regulated. These antigens have served as useful markers for cell identification and isolation of several neural cell types. The molecular nature and functional properties of almost all of these antigens are presently unknown.

Animals↗
PubMed2004

Correlations among neural cell adhesion molecule, nerve growth factor, and its receptors, TrkA, TrkB, TrkC, and p75, in perineural invasion by basal cell and cutaneous squamous cell carcinomas.

BACKGROUND: Neural cell adhesion molecule; nerve growth factor; and its receptors TrkA, TrkB, TrkC, and p75(NGFR) regulate unique survival pathways in the cells of different noncutaneous malignancies exhibiting a perineural invasive phenotype. Their expression is currently unknown in basal cell carcinoma and cutaneous squamous cell carcinoma exhibiting perineural invasion. OBJECTIVE: The objective was to evaluate neural cell adhesion molecule, nerve growth factor, TrkA, TrkB, TrkC, and p75(NGFR) expression when perineural invasion occurs in basal cell carcinoma and cutaneous squamous cell carcinoma. METHODS: Four basal cell carcinomas and five cutaneous squamous cell carcinomas that were perineural invasion-positive and four basal cell carcinomas and three cutaneous squamous cell carcinomas that were perineural invasion-negative were evaluated for the expression of neural cell adhesion molecule, nerve growth factor, TrkA, TrkB, TrkC, and p75(NGFR) by immunohistochemical staining. RESULTS: For neural cell adhesion molecule, six of eight basal cell carcinomas and two of eight cutaneous squamous cell carcinomas stained positive. For nerve growth factor, seven of nine perineural invasion-positive and six of seven perineural invasion-negative tumors stained moderately or greater. For TrkA, B, and C, the perineural invasion-positive cutaneous squamous cell carcinomas generally stained darker than the perineural invasion-negative cutaneous squamous cell carcinomas. For p75(NGFR), four of five perineural invasion-positive cutaneous squamous cell carcinoma stain patterns indicated that p75(NGFR) expression was higher perineurally than elsewhere in the tumor. CONCLUSION: In basal cell carcinoma and cutaneous squamous cell carcinoma, the presence of neural cell adhesion molecule may determine tumor aggression and increased levels of nerve growth factor and TrkA, B, and C may reflect unique survival pathways. Higher levels of expression of Trk receptors in cutaneous squamous cell carcinoma cells may predict perineural invasion and the increased p75(NGFR) expression found in cutaneous squamous cell carcinoma perineurally may allow p75(NGFR) immunohistochemical staining to be used for detecting sites of perineural invasion.

Aged↗
PubMed1998

Treatment of neurodegenerative diseases with neural cell transplantation.

Neural cell transplantation is an emerging therapy that may provide an effective treatment for neurodegenerative disorders. The most extensive work with neural transplants has been carried out for Parkinson's and Huntington's diseases. However, intensive efforts are also being made for the treatment of other neurological indications, such as spinal cord repair, stroke, epilepsy, multiple sclerosis (MS), Alzheimer's disease and amyotrophic lateral sclerosis (ALS or Lou Gehrig's disease), to name just a few. The major barrier for the successful application of cells as therapeutics is achieving long-term survival and function. The CNS has proven to be ideal for transplantation, in part because immune rejection is attenuated in the CNS compared to peripheral locations. However, some form of immunosuppression is desirable for optimal allograft survival and required for xenograft survival. This review will focus on the challenges of restoring function to something as intricate as the CNS and on the limitations imposed by this complexity on any cellular therapeutic.

Journal Article↗
PubMed1993

Neuronal 'differentiation' of murine neuroblastoma cells induced by neocarzinostatin: neural cell adhesion molecules.

Neural crest tumor cells which have been pharmacologically induced in culture to undergo neuronal 'differentiation' have been proposed as a model for normal neural crest cell differentiation. We have previously reported that murine neuroblastoma cells treated with the antineoplastic agent neocarzinostatin (NCS) adopt the light microscopic appearance of differentiated neurons. After undergoing morphologic change, the cells no longer divide. As part of an effort to compare the process of differentiation in these cells with what is known about normal neural crest cells, we have examined the cellular distribution and isoform complement of neural cell adhesion molecules (NCAMs) in native and NCS-treated neuroblastoma cells. Our studies show that NCS induces profound changes in NCAM distribution. Immunohistochemical staining indicates that, in contrast to native neuroblastoma cells, more than 80% of treated cells display surface NCAM by 4 days following treatment. Unlike the case for normal neurons, NCAM is uniformly distributed over the treated cell surface. Neuroblastoma cells treated with NCS are more avidly adherent to culture plates coated with NCAM than are control neuroblastoma cells, reflecting the homophilic binding characteristics of NCAM. Interestingly, Western blot analysis for NCAM demonstrates similar total cellular content of a single NCAM species in both control and treated neuroblastoma cells. Furthermore, this 120 kDa mol. wt. NCAM is an isoform of NCAM not found on normally differentiated cerebellar neurons. While the presence of NCAM on these treated murine neuroblastoma cells is evidence for 'differentiation' along neuronal lines, the isoform complement and cell surface distribution of NCAM in treated cells are not normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Molecular association of two neural cell adhesion molecules within the surface membrane of cultured mouse neuroblastoma cells.

The neural cell adhesion molecule L1 can be induced by antibodies in indirect immunofluorescence procedures to co-redistribute on the surface membrane of cultured mouse neuroblastoma cells with the 180 kDa component of N-CAM, but not with the 140 kDa component of N-CAM, the H-2 histocompatibility antigen or antigens recognized by polyspecific antibodies to mouse liver membranes. These observations indicate a differential and close molecular association between L1 and the N-CAM component with the larger intracellular domain.

Animals↗
PubMed2005

Systems analysis of RNA trafficking in neural cells.

In neural cells, certain RNAs are targeted to dendrites by a specific RNA trafficking pathway, termed the A2 pathway, mediated by the trans-acting trafficking factor, heterogeneous nuclear ribonucleoprotein (hnRNP) A2, which binds to an 11 nucleotide cis-acting trafficking sequence, termed the hnRNP A2 response element (A2RE). RNAs containing A2RE-like sequences are recognized by hnRNP A2 in the nucleus and exported to the cytoplasm where they assemble into trafficking intermediates, termed granules, which also contain components of the translation machinery and molecular motors (cytoplasmic dynein and conventional kinesin). RNA granules move along microtubules to the cell periphery where they become localized and where the encoded protein is translated. Intracellular trafficking of RNA molecules by the A2 pathway is mediated by a complex system consisting of five different subsystems, approximately 35 different molecules and approximately 45 different molecular interactions. Specificity in the A2 pathway is provided by specific interactions of hnRNP A2 with different molecular partners in different subsystems. Polarity of RNA trafficking is controlled by transitions of trafficking intermediates between different subsystems. Comprehensive understanding of the A2 RNA trafficking pathway will require quantitative analysis of concentrations and diffusion constants for each of the different molecules, on rates and off rates for each of the different interactions, relevant conditional operators controlling specific interactions, and interactions of different subsystems. Once the necessary quantitative data are available, mathematical models for the different RNA trafficking subsystems can be developed using computational platforms such as the 'Virtual Cell'. Here we describe how each of the subsystems in the A2 system functions and how the different subsystems interact to regulate RNA trafficking.

Animals↗
PubMed2001

In vitro differentiation of human marrow stromal cells into early progenitors of neural cells by conditions that increase intracellular cyclic AMP.

Human marrow stromal cells (hMSCs) are multipotential stem cells that can be differentiated into bone, cartilage, fat, and muscle. In the experiments here, we found that undifferentiated cultures of hMSCs express some markers characteristic of neural cells such as microtubule-associated protein 1B (MAP1B), neuron-specific tubulin (TuJ-1), neuron-specific enolase (NSE), and vimentin. By treating hMSCs with 0.5 mM isobutylmethylxanthine (IBMX)/1 mM dibutyryl cyclic AMP (dbcAMP) for 6 days, about 25% of the hMSCs differentiated into cells with a typical neural cell morphology and with increased levels of both NSE and vimentin. The data suggested that the hMSCs may have been differentiated into early progenitors of neural cells in vitro under conditions that increase the intracellular level of cAMP.

1-Methyl-3-isobutylxanthine↗
PubMed2006

Neudesin, a secreted factor, promotes neural cell proliferation and neuronal differentiation in mouse neural precursor cells.

Neudesin encodes a secreted signal with neurotrophic activity in neurons. Most neurotrophic factors are involved in neural cell proliferation and/or differentiation. However, the role of neudesin in neural development remains to be elucidated. We examined the expression of neudesin in mouse embryonic cerebral cortex and cultured mouse neural precursor cells and its roles in neural development. Neudesin was expressed in the embryonic cerebral cortex early in development. Its expression was observed mainly in the preplate, where mostly postmitotic neural cells existed. Because neudesin mRNA was expressed in the neural precursor cells before the appearance of neurons, the roles of neudesin in neural development were examined by using the precursor cells. Neudesin significantly promoted neuronal differentiation and overrode the undifferentiated state of the neural precursor cells sustained by fibroblast growth factor 2 (FGF2). In contrast, it inhibited the differentiation of astrocytes. In addition, neudesin transiently promoted neural cell proliferation early in the developmental process. The effect on cell proliferation was distinct from that of FGF2, a self-renewal-promoting factor for neural precursor cells. The differentiation was mediated though activation of the protein kinase A (PKA) and phosphatidylinositol-3 kinase (PI-3K) pathways. In contrast, the proliferation was mediated through the mitogen-activated protein kinase and PKA pathways. The expression profile and activity indicate that neudesin plays unique roles in neural development. The present findings have revealed new potential roles of neudesin in neural cell proliferation and neuronal differentiation.

Animals↗
PubMed2006

[Human amnion cells express the phenotypes of neural cells and adipocytes in vitro].

OBJECTIVE: To search for culture conditions in which the cells from human amnion could diferentiate into neural cells and hence to explore a new cell source for neural transplantaion. METHODS: Amnion cells from human were cultured with tissue piece method, passaged by trypsin digestion and identified with immunocytochemistry. RESULTS: Amnion cells migrated from explants and primary culture was established; they could multiply and expand steadily in a short time, and they could be passaged by trypsin digestion. When cultured in serum-free neural stem cell media, these cells could form the same spheroid shape as the neurospheres of neural stem cells. They could express alpha smooth muscle actin and differentiate into smooth muscle cells spontaneously, and could express nestin and vimentin, the markers for neural progenitors. Moreover, they could he stained by anti-beta III-tubulin, anti-neurofilament 200 and anti-NSE; the majorities could he stained by antityrosine hydroxylase, the marker for dopaminergic neurons. Lower than 0.1% of the total cells were stained by GFAP, indicating the existence of astrocytes. The amnion cells could also differentiate into adipocytes under specific induction. CONCLUSION: Amnion cells could differentiate into adipocytes and smooth muscle cells; they could express the protein for neural cells; thus may represent an alternative stem cell source for CNS cell transplantation.

Adipocytes↗
PubMed1993

Expression of insulin-like growth factor binding protein-4 (IGFBP-4) by rat neural cells--comparison to other IGFBPs.

We recently isolated and characterized the 24 kDa and N-glycosylated 28 kDa insulin-like growth factor binding protein-4 (rIGFBP-4) from the B104s rat neuronal cell line (Endocrinology, 129 (1991) 1009-1115). To examine the prevalence of IGFBP-4 secretion by cells of neural origin, we assessed the expression of IGFBP-4 in different neural cell types using ligand blotting, immunoblotting and blot hybridization with relevant cDNAs. A specific IGFBP-4 antibody raised against a synthetic 20 amino acid peptide was used for immunologic recognition. In all the neural cells tested (B104s, C6 astrocytoma, primary neonatal astrocytes and primary fetal neurons), IGFBP-4 was definitively identified by immunoblotting. Blot hybridization using a rat cDNA probe revealed expression of IGFBP-4 mRNA transcripts by all these cells. Using a combination of the same techniques, expression of IGFBP-1, -2, and -3 were also examined. The B104s cells secreted primarily IGFBP-4; C6 cells secreted predominantly IGFBP-3 and small amount of IGFBP-4; both primary neonatal astrocytes and fetal neurons secreted IGFBP-2 as the major IGFBP accompanied by a small quantity of IGFBP-4. IGFBP-1 was not identified in any of the cell media. When probed with the respective IGFBP cDNAs, the mRNA abundance generally reflected the media IGFBP content. The expression of IGFBP-4 mRNA in vivo was examined as well and compared to that of IGFBP-1 and IGFBP-2. Transcripts for both IGFBP-2 and IGFBP-4 were found in all gross anatomical divisions of the rat brain from embryonic day 15 until adulthood, whereas IGFBP-1 was not detected at any time. IGFBP-4 mRNA tended to be more abundant at the youngest ages whereas IGFBP-2 increased during development. These data indicate that IGFBP-4 is produce by a variety of neural cell types and suggest that it may play a role in brain development.

Amino Acid Sequence↗
PubMed2002

In vitro differentiation of size-sieved stem cells into electrically active neural cells.

Size-sieved stem (SS) cells isolated from human bone marrow and propagated in vitro are a population of cells with consistent marker typing, and can form bone, fat, and cartilage. In this experiment, we demonstrated that SS cells could be induced to differentiate into neural cells under experimental cell culture conditions. Five hours after exposure to antioxidant agents (beta-mercaptoethanol +/- retinoic acid) in serum-free conditions, SS cells expressed the protein for nestin, neuron-specific enolase (NSE), neuron-specific nuclear protein (NeuN), and neuron-specific tubulin-1 (TuJ-1), and the mRNA for NSE and Tau. Immunofluorescence showed that almost all the cells (>98%) expressed NeuN and TuJ-1. After 5 days of beta-mercaptoethanol treatment, the SS cells expressed neurofilament high protein but not mitogen-activated protein-2, glial filament acidic protein, and galactocerebroside. For such long-term-treated cells, voltage-sensitive ionic current could be detected by electrophysiological recording, and the intracellular calcium ion, Ca(2+), concentration can be elevated by high potassium (K(+)) buffer and glutamate. These findings suggest that SS cells may be an alternative source of undifferentiated cells for cell therapy and gene therapy in neural dysfunction.

Antineoplastic Agents↗
PubMed2004

ShcA regulates neurite outgrowth stimulated by neural cell adhesion molecule but not by fibroblast growth factor 2: evidence for a distinct fibroblast growth factor receptor response to neural cell adhesion molecule activation.

Homophilic binding in trans of the neural cell adhesion molecule (NCAM) mediates adhesion between cells and leads, via activation of intracellular signaling cascades, to neurite outgrowth in primary neurons as well as in the neuronal cell line PC12. NCAM mediates neurite extension in PC12 cells by two principal routes of signaling: NCAM/Fyn and NCAM/fibroblast growth factor receptor (FGFR), respectively. Previous studies have shown that activation of mitogen-activated protein kinases is a pivotal point of convergence in NCAM signaling, but the mechanisms behind this activation are not clear. Here, we investigated the involvement of adaptor proteins in NCAM and fibroblast growth factor 2 (FGF2)-mediated neurite outgrowth in the PC12-E2 cell line. We found that both FGFR substrate-2 and Grb2 play important roles in NCAM as well as in FGF2-stimulated events. In contrast, the docking protein ShcA was pivotal to neurite outgrowth induced by NCAM, but not by FGF2, in PC12 cells. Moreover, in rat cerebellar granule neurons, phosphorylation of ShcA was stimulated by an NCAM mimicking peptide, but not by FGF2. This activation was blocked by inhibitors of both FGFR and Fyn, indicating that NCAM activates FGFR signaling in a manner distinct from FGF2 stimulation, and regulates ShcA phosphorylation by the concerted efforts of the NCAM/FGFR as well as the NCAM/Fyn signaling pathway.

Adaptor Proteins, Signal Transducing↗
PubMed2004

Overexpression of neural cell adhesion molecule in regenerative muscle fibers in 3-hydroxy-3-methylglutaryl coenzyme: A reductase inhibitor-induced rhabdomyolysis.

Skeletal muscle degeneration is a side effect of cholesterol-lowering hydroxymethylglutaryl coenzyme A reductase inhibitors. The expression of the cell-cell adhesion proteins, neural cell adhesion molecule and neural-cadherin was studied in a case of rhabdomyolysis induced by the hydroxymethylglutaryl coenzyme A reductase inhibitor cerivastatin. Neural cell adhesion molecule and N-cadherin participate in the interactions of muscle cells during skeletal myogenesis. In the adult muscle, neural cell adhesion molecule is restricted to neuromuscular sites but is re-expressed in denervated muscle and in rhabdomyolysis. Our results show expression of neural cell adhesion molecule in regenerative skeletal muscle fibers but not in degenerated or unaffected fibers in cerivastatin-induced rhabdomyolysis. In contrast, N-cadherin was not expressed. The presence of apoptotic cells was studied by a fluorescence-based Tdt-mediated dUTP nick-end labeling in the same sections. Apoptosis was detected in degenerative fibers and inflammatory cells but not in regenerative fibers. We hypothesize that the expression of neural cell adhesion molecule in regenerative fibers may have a protective role against apoptosis during rhabdomyolysis. Cerivastatin-induced rhabdomyolysis appears to have common features with rhabdomyolysis of other causes. The immunohistochemical study of neural cell adhesion molecule can serve as an additional tool in the evaluation of muscle regeneration in rhabdomyolysis.

Aged↗
PubMed1982

Effect of exogenous gangliosides on human neural cell division.

Human neural cells in exponential growth phase were transferred to a serum-free medium and maintained for 72 hr without any detectable loss in viability. The two normal fetal cell lines (CHI and CHII) showed a serum-dependent cell proliferation, but the glioblastoma multiforme cells (12-18) were able to continue proliferating in this totally synthetic medium. The incorporation of [3H]thymidine into the acid-precipitable fraction of both normal and neoplastic human neural cells was assayed in the presence and the absence of exogenous gangliosides by a convenient new method. In serum-free medium, gangliosides (50 microM) inhibited the thymidine incorporation into the normal fetal cells within 24 hr and, in serum containing medium, reduced their proliferation within 48 hr. No such effects were detectable in the glioma cells. The inhibition of thymidine incorporation in the normal cells was reversible upon removal of the gangliosides. These results indicate a role of gangliosides in the postmitotic phase of normal human neural cells resulting in the regulation of cell proliferation.

Brain↗