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PubMed1996

P2-purigenic receptors regulate phospholipase C and adenylate cyclase activities in immortalized Schwann cells.

Schwann cells play an important role in both the development and regeneration of peripheral nerves. Proliferation and differentiation of Schwann cells are critically dependent on changes in the levels of cAMP. ATP is a fast excitatory transmitter in the peripheral nervous system, inducing depolarization of the vagus nerve through occupancy of P2-purinergic receptors. In the present study we demonstrate that extracellular ATP stimulates phospholipase C and inhibits adenylate cyclase activities in cultured Schwann cells. Addition of ATP inhibited, in a concentration-dependent manner, forskolin- or isoprenaline-stimulated adenylate cyclase activity. The rank order of potency corresponding to different purinergic receptor agonists was 2-methylthio-ATP > ATP = ADP > or = adenosine 5'-[gamma-thio]triphosphate (ATP[S]) > UTP, consistent with the involvement of a P2y subtype. Adenosine and adenosine 5'-[alpha,beta-methylene]-triphosphate (pp[CH2pA) were ineffective. Preincubation with pertussis toxin completely blocked this inhibitory effect. When Schwann cells were pre-labelled with myo-[3H]inositol and incubated in Hanks' balanced salt solution containing Ca2+ and Mg2+, addition of ATP[S] resulted in a concentration-dependent increase in the release of InsP with a concomitant increase in intracellular free [Ca2+] ([Ca2+]i). Under these conditions, the effects of both ATP and UTP were of lower magnitude. Removal of Ca2+ and Mg2+ from the assay medium resulted in a significant increase in the effects of ATP[S], ATP and UTP. The decreased response observed in the presence of both bivalent cations (1.2 mM Ca2+ and 1 mM Mg2+) could not be explained either by increased degradation of ATP by Ca2+/Mg2+-dependent nucleotidases or by cation influx. The rank order of potency for the effects of agonists on phospholipase C activity was ATP[S] = adenosine 5'[gamma-imido]triphosphate > ATP -UTP > ADP, indicating the involvement of a P(2U) receptor subtype in this response. Adenosine, AMP and pp[CH2]pA were ineffective. These results demonstrate that immortalized Schwann cells express P(2U) and P(2Y) purinoceptors, which are coupled to stimulation of phospholipase C and inhibition of adenylate cyclase, respectively. Our observations unveil signal-transduction pathways that may be used by ATP to regulate proliferation and differentiation of Schwann cells, and ultimately to influence nerve homeostasis.

Adenosine Triphosphatases↗

PubMed1998

Neuronal survival: early dependence on Schwann cells.

Schwann cells fail to develop in mouse embryos lacking functional ErbB3 neuregulin receptors, and most sensory and motor neurons subsequently die in these mice. As ErbB3 acts cell autonomously in Schwann cell development but not in neuronal survival, neurons may depend on Schwann cells for survival.

Animals↗

PubMed1997

The expression of the low affinity nerve growth factor receptor in long-term denervated Schwann cells.

Schwann cells in the distal stump of injured peripheral nerves synthesize the low affinity nerve growth factor receptor (p75). In this study we used short-term (1 week) and long-term (1-12 months) transected distal sciatic nerves of rats to determine the variations of p75 expression by using immunocytochemistry and in situ hybridization. Semi-quantitative analysis revealed that the synthesis of the protein product of the p75 gene is rapidly enhanced to reach a peak within the 1 month after denervation. After that it gradually decreased and was barely detectable 6 months following denervation. Double immunocytochemistry for p75 and the S100 protein revealed that p75 immunoreactivity is confined to the Schwann cells. Quantitative analysis of our in situ hybridization experiments revealed that the upregulation of the p75 mRNA parallels the enhanced synthesis of the corresponding protein and reaches a peak within 1 month, which is maintained until the second month after the transection and declines thereafter to reach background levels at 4 months. The electron microscopic observations reveal that the increase in the number of nuclei in the distal stump belong to severely atrophied Schwann cells and fibroblasts. Since the presence of p75 in the Schwann cells is necessary for reinnervation, our results indicate that, based on the expression of p75, the Schwann cells will provide a most suitable environment for the regenerating axons up to the first month. At later stages the ability of the Schwann cells to synthesize p75 and cell adhesion proteins such as N-CAM and GAP 43 decreases which may be one of the factors that contribute to poor functional recovery if the regenerating axons reach the distal stump after long periods of time.

Animals↗

PubMed1997

Induction of LIF-mRNA by TGF-beta 1 in Schwann cells.

Schwann cell is a cell type that forms myelin sheath and provides trophic supports for neuronal cells by producing neurotrophic factors such as neurotrophins and neurokines in both normal and traumatic situations. It was recently reported that after lesion of sciatic nerve, mRNA for cholinergic differentiation factor (CDF)/leukemia inhibitory factor (LIF) is induced in nonneuronal cells in the nerve. However, the source of LIF-mRNA and the mechanism of LIF-mRNA regulation have remained largely unknown. In the present study, we searched for factors regulating the LIF-mRNA expression in cultured Schwann cells isolated from newborn rat sciatic nerve. Among various growth factors and cytokines tested, TGF beta-1 exerted the most prominent effect on the induction of LIF-mRNA in the cultured Schwann cells. The effect of TGF-beta 1 on the increase of LIF-mRNA levels was suppressed by either staurosporine or H-7 suggesting the role of PKC or PKC-like protein kinase activity in the induction of LIF-mRNA. The induction of LIF mRNA by TGF-beta 1 was suppressed in the co-culture of the Schwann cells with embryonic rat DRG neurons. The addition of ascorbic acid, which is known to promote myelination in this co-culture system, further suppressed the TGF-beta 1 induction of LIF-mRNA. These results suggest that Schwann cells respond to TGF-beta 1 in a lesion situation to produce LIF, which supports neuronal survival and regeneration. The re-establishment of neuron-Schwann cell interaction would in turn suppress the LIF production to terminate its action during the lesion situation.

Age Factors↗

PubMed2002

The early life of a Schwann cell.

Schwann cells are the major glial population of the vertebrate peripheral nervous system. In the adult, they build a protecting sheath around neuronal processes and myelinate large-caliber axons. Already early in development, Schwann cells and neurons establish close contacts. Later development and the maintenance of peripheral nerves are crucially dependent on the controlled bi-directional dialogue between these two cell types. Several major phases can be distinguished in the life of a Schwann cell: determination, differentiation, and potentially myelination. The aim of this review is to summarize the molecular and cellular characteristics of the first steps in the life of a Schwann cell, the development from a multipotent neural crest cell to a differentiated Schwann cell.

Animals↗

PubMed1982

Demonstration of 2',3'-cyclic nucleotide 3'-phosphohydrolase in cultured human Schwann cells.

Schwann cell cultures were established from adult human sural nerve biopsies. 2'3'-Cyclic nucleotide 3'-phosphohydrolase (CNPase) activity was estimated in the homogenates of those cells by a sensitive isotope assay using [3H]2',3'-cyclic AMP as substrate. A high level of CNPase activity was observed in cultured Schwann cells, whereas cultured human muscle and skin fibroblasts contained negligible levels of CNPase activity. CNPase of human Schwann cells followed typical enzyme-substrate kinetics, with an apparent Km of 1.6 mM for 2',3'-cyclic AMP, and the enzyme was stimulated by detergents such as Triton X-100 and deoxycholate. It was inhibited by p-chloromercuricbenzoate and 2'-AMP. These properties are typical of CNPase isolated from adult brain and spinal cord. CNPase can serve as a new biochemical marker of normal cultured human Schwann cells and can be useful in analyzing the properties of cultured Schwann cells from patients with dysschwannian neuropathies.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗

PubMed2006

Reconstitution of the NF1 GAP-related domain in NF1-deficient human Schwann cells.

Schwann cells derived from peripheral nerve sheath tumors from individuals with Neurofibromatosis Type 1 (NF1) are deficient for the protein neurofibromin, which contains a GAP-related domain (NF1-GRD). Neurofibromin-deficient Schwann cells have increased Ras activation, increased proliferation in response to certain growth stimuli, increased angiogenic potential, and altered cell morphology. This study examined whether expression of functional NF1-GRD can reverse the transformed phenotype of neurofibromin-deficient Schwann cells from both benign and malignant peripheral nerve sheath tumors. We reconstituted the NF1-GRD using retroviral transduction and examined the effects on cell morphology, growth potential, and angiogenic potential. NF1-GRD reconstitution resulted in morphologic changes, a 16-33% reduction in Ras activation, and a 53% decrease in proliferation in neurofibromin-deficient Schwann cells. However, NF1-GRD reconstitution was not sufficient to decrease the in vitro angiogenic potential of the cells. This study demonstrates that reconstitution of the NF1-GRD can at least partially reverse the transformation of human NF1 tumor-derived Schwann cells.

Base Sequence↗

PubMedDate not supplied

Electrophysiology of mammalian Schwann cells.

Schwann cells are the satellite cell of the peripheral nervous system, and they surround axons and motor nerve terminals. The review summarises evidence for the ion channels expressed by mammalian Schwann cells, their molecular nature and known or speculated functions. In addition, the recent evidence for gap junctions and cytoplasmic diffusion pathways within the myelin and the functional consequences of a lower-resistance myelin sheath are discussed. The main types of ion channel expressed by Schwann cells are K(+) channels, Cl(-) channels, Na(+) channels and Ca(2+) channels. Each is represented by a variety of sub-types. The molecular and biophysical characteristics of the cation channels expressed by Schwann cells are closely similar or identical to those of channels expressed in peripheral axons and elsewhere. In addition, Schwann cells express P(2)X ligand-gated ion channels. Possible in vivo roles for each ion channel type are discussed. Ion channel expression in culture could have a special function in driving or controlling cell proliferation and recent evidence indicates that some Ca(2+) channel and Kir channel expression in culture is dependent upon the presence of neurones and local electrical activity.

Animals↗

PubMed1986

A cytoskeleton-associated plasma membrane heparan sulfate proteoglycan in Schwann cells.

Schwann cells cocultured with sensory neurons in a serum-free medium accumulate a single species of radiolabeled heparan sulfate proteoglycan (HS-PG) during incubation in medium containing 35SO4. This HS-PG was poorly extracted from cultures by solutions containing 1% Triton X-100 in low salt buffer or by solutions containing 1 M KCl, 4 M urea plus dithiothreitol, 1 mM Tris-HCl, 5 mM EDTA, or 100 micrograms/ml of heparin. The HS-PG was efficiently extracted, however, by 1% Triton X-100 in the presence of 1 M KCl or by 1% deoxycholate. These treatments solubilize both cell membranes and the Schwann cell cytoskeleton. In intact cells the HS-PG was digested by trypsin, indicating it was at least partially exposed on the cell surface. When solubilized HS-PG was applied to a column of octyl-sepharose CL-4B, more than 90% was retained by the column, but was quantitatively eluted by a solution containing 1% Triton X-100. In addition, the solubilized HS-PG could be incorporated into artificial phospholipid vesicles. These results indicate the HS-PG is an integral plasma membrane protein. The inability of low ionic strength solutions containing Triton X-100 to solubilize the HS-PG suggested it was bound to an additional structure. To determine whether the HS-PG was associated with the cytoskeleton we isolated cytoskeletons by detergent lysis of cells and centrifugation. The major protein components of isolated cytoskeletons were spectrin (Mr 225,000), vimentin (Mr 58,000), and actin (Mr 45,000). When 35SO4-labeled cells were used to prepare cytoskeletons approximately 80% of the total HS-PG was recovered in the cytoskeleton fraction. These results suggest the HS-PG is an externally exposed integral plasma membrane protein that is anchored to the Schwann cell cytoskeleton.

Animals↗

PubMed1999

DMSO induction of the leukotriene LTC4 by Lewis rat Schwann cells.

Schwann cells are capable of producing many immunomodulatory molecules, which indicates that they may play an active role in autoimmune diseases of the peripheral nervous system. We have previously reported production of the prostanoids prostaglandin E2 and thromboxane A2, products of arachidonic acid metabolism, by Schwann cells. This study reports that Schwann cells are capable of producing leukotriene C4, also a product of arachidonic acid metabolism. Production of leukotriene C4 was in response to pre-incubation of the Schwann cells with the cytokines interferon-gamma and tumour necrosis factor-alpha followed by incubation with dimethylsulfoxide. The cytokines alone did not elicit a response nor did stimulation with calcium ionophore, phorbol ester or lipopolysaccharide.

Animals↗

PubMed2003

Autocrine action of BMP2 regulates expression of GDNF-mRNA in sciatic Schwann cells.

Schwann cell is a cell type that forms myelin sheath and provides trophic supports for neuronal cells by producing neurotrophic factors in both normal and traumatic situations. It was recently reported that after lesion of sciatic nerve, mRNA for glial cell line-derived neurotrophic factor (GDNF) is induced in nonneuronal cells in the nerve. However, the mechanism regulating GDNF-mRNA has remained largely unknown. In the present study, we searched for factors regulating the GDNF-mRNA expression in Schwann cells. First, we found that after transfer into explant culture as an in vitro lesion model, sciatic nerve segments began to express mRNA for bone morphogenetic protein-2 (BMP2) concomitantly with the induction of GDNF-mRNA. Treatment of the Schwann cells isolated from the sciatic nerve with combination of BMP2 and retinoic acid (RA) dramatically induced GDNF-mRNA, while BMP2 or RA alone had no effect. Furthermore, ionomycin, a calcium ionophore, which had even stronger activity on the induction of GDNF-mRNA also induced also BMP2-mRNA in cultured Schwann cells. Effects of inhibitors of intracellular signaling pathways such as protein kinase C inhibitor and MAPKK inhibitor suggested that the molecular mechanism of the induction of GDNF-mRNA is distinct from that of BMP2-mRNA. These results suggest that the Schwann cell-produced BMP2 plays an important role in the induction of GDNF after nerve injury in an autocrine fashion.

Animals↗

PubMed1985

Experimental lead neuropathy: inorganic lead inhibits proliferation but not differentiation of Schwann cells.

Schwann cells were prepared from the sciatic nerves of newborn rats and cultured in a monolayer. Addition of lead acetate at concentrations between 0.4 and 10.0 micrograms/ml, levels comparable to those occurring in neural tissues and physiological fluids of lead-intoxicated rats, diminished both the baseline rate of proliferation of the Schwann cells and their response to the mitogens, axolemmal fragments, glial growth factor, and the adenosine 3':5'-cyclic monophosphate (cAMP) analogues 8-bromo-cAMP and dibutyryl-cAMP. This demonstrates a direct toxic effect of inorganic lead on Schwann cells. Lead acetate in this concentration range did not, however, inhibit the cAMP analogue-induced appearance of the "myelin marker" lipid galactocerebroside on the surfaces of the cultured Schwann cells.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1997

The neural cell recognition molecule F11 is expressed on Müller cells and Schwann cells in vitro.

The neural cell recognition molecule F11 is a member of the immunoglobulin superfamily. During development it is expressed on axons in neuropils, and it is implicated in neurite outgrowth and in fasciculation. F11 is a multifunctional protein that interacts with L1/Ng-CAM, Nr-CAM, tenascin-C, tenascin-R (restrictin) and receptor protein tyrosine phosphatase beta. Here we show that F11 is not only expressed on neurons, but also on Müller cells and Schwann cells in vitro. Using two independent cell culture techniques, stratospheroids which represent an in vitro regeneration system of the chicken retina, and purified Schwann cells from chicken sciatic nerve, we show that Müller cells and Schwann cells express F11. On semithin cryosections of stratospheroids we were able to colocalize F11 with the Müller cell markers vimentin and 3A7. Expression of F11 by purified Schwann cells in demonstrated histologically and by immunoblot analysis. These in vitro data suggest the involvement of F11 in glia-neuron or glia-neurite interactions.

Animals↗

PubMed1992

Interactions between CD4+ T-cells and rat Schwann cells in vitro. 1. Antigen presentation by Lewis rat Schwann cells to P2-specific CD4+ T-cell lines.

Interactions between CD4+ P2-specific T-cell lines and Schwann cells were examined in vitro by scanning electron microscopy (SEM) and T-cell proliferation studies. CD4+ T-cell lines clustered around and attached to Schwann cells which expressed Major histocompatibility complex (MHC) class II molecules. Only those P2-specific T-cell lines capable of inducing experimental allergic neuritis (EAN) when injected into adult Lewis rats clustered around the Schwann cells. T-cell lines responsive to P2 but not able to induce EAN did not cluster around Schwann cells. The addition of exogenous P2 protein inhibited in a dose-dependent way clustering and proliferation of the P2-specific T-cell lines. Cytoplasmic P2 was detected in Schwann cells by immunofluorescent labelling and the results of proliferation assays in this study suggest that endogenous P2 protein was processed by the Schwann cells and presented to T-cell lines in association with MHC class II molecules. The clustering and proliferation of class II-restricted CD4+ P2-specific T-cell lines in the presence of Schwann cells provides evidence for a role for Schwann cells as facultative antigen presenting cells, processing and presenting 'self' endogenous antigen to CD4+ T-cell lines capable of inducing EAN.

Animals↗

PubMed1990

Possible precursors to new hair cells, support cells, and Schwann cells in the ear of a post-embryonic fish.

The sources of new hair cells, support cells, and Schwann cells were identified in the statoacoustic end organs of normal post-embryonic fish (Astronotus ocellatus). S-phase cells, defined as cells that take up 3H-thymidine in preparation for mitosis, and their progeny were visualized using autoradiography. Two types of S-phase cells were found: 'embryonic-like neuroepithelial' (NE) cells and 'basally located S-phase' (BLS) cell. The NE cells had elongated nuclei and processes extending basally and apically. Thirty minutes after the thymidine injection labeled NE cell nuclei were found between hair cell nuclei and support cell nuclei. After two and four hours survival some labeled NE nuclei were closer to the lumen, where they divided. One labeled support cell was seen after four hours survival and one labeled hair cell after nine hours survival. Significant numbers of labeled support and hair cells were not seen until 24 h survival. These results led us to identify NE cells as the immediate source of new hair cells and support cells. The BLS cells had small nuclei with little surrounding cytoplasm. Shortly after the thymidine injection BLS cells were found between the hair cell nuclei and the basement membrane, and they underwent mitosis in this position. The BLS cells resemble intra-epithelial Schwann cells, except that they are not curved around axonal profiles. We suggest that the BLS cells are Schwann cell precursors.

Animals↗

PubMed1987

Comparison of the Schwann cell surface and Schwann cell extracellular matrix as promoters of neurite growth.

The ability of Schwann cells to influence the direction and rate of neurite growth was investigated in a tissue culture model of the bands of Büngner of injured peripheral nerve. The arrangement of this culture system allowed testing of the growth-promoting properties of the Schwann cell surface and extracellular matrix (ECM) assembled by Schwann cells rather than soluble substances secreted into conditioned medium. Various components of peripheral nerve were examined separately as substrata for regenerating neurites: (i) Schwann cells and their ECM; (ii) Schwann cells alone; (iii) Schwann cell ECM alone; (iv) Schwann cells, fibroblasts, and their assembled ECM; (v) Schwann cells, their ECM and neurites; and (vi) purified laminin. Regenerating peripheral neurites were from explants of foetal rat dorsal root ganglia, which had been cultured for several weeks to rid them of accompanying non-neuronal cells, or from explants of foetal rat superior cervical ganglia, which contained non-neuronal cells. CNS neurites from the somatosensory cortex of embryonic rats were also studied; these neurites may be either first growing or regenerating. Neurites from all types of explants studied grew longer and were guided on a substratum of Schwann cells or Schwann cell ECM compared with a collagen substratum. The presence of fibroblasts during ECM assembly did not enhance the neurite growth-promoting activity. The design of the experiments suggested that the factors by which the Schwann cells or their ECM promoted and guided neurite outgrowth were surface-bound rather than medium-borne. Electron microscopic examination showed that neurites grew on either Schwann cell surfaces or basal lamina material. Attempts to define the chemical nature of the neurite growth-promoting effect of ECM by partial enzymatic digestion did not identify any single component as essential. Purified laminin was a more effective promoter of outgrowth of peripheral neurites than were Schwann cells or Schwann cell ECM. Cortical explants also grew on laminin, but neurites were accompanied on this substratum by a massive migration of non-neuronal cells; the neurites appeared to extend primarily on the non-neuronal cells rather than by direct attachment to the laminin substratum. This characteristic outgrowth of cortical non-neuronal cells on laminin was not consistently seen on Schwann cell ECM. In conclusion, either the Schwann cell surface or the ECM produced and assembled by Schwann cells promotes neurite outgrowth and guides that outgrowth from the several types of peripheral and CNS neurons studied in this report.

Animals↗

PubMed1992

Interactions between CD4+ T-cells and rat Schwann cells in vitro. 2. Cytotoxic effects of P2-specific CD4+ T-cell lines on Lewis rat Schwann cells.

The cytotoxic effects of CD4+ P2-specific T-cell lines on Schwann cells were examined in vitro with 51Cr-release cytotoxicity assays. Only those P2-specific T-cell lines capable of inducing EAN when injected back into adult Lewis rats were cytotoxic to the Schwann cells. The addition of exogenous P2 protein was not necessary for the cytotoxic effect. The monoclonal antibody (mAb) OX6 directed against Major histocompatibility complex (MHC) class II molecules blocked cytotoxicity, indicating an essential role for MHC class II molecules in this interaction between CD4+ T-cell lines and Schwann cells.

Animals↗

PubMed1995

A Mycobacterium leprae gene encoding a fibronectin binding protein is used for efficient invasion of epithelial cells and Schwann cells.

Mycobacterium leprae, the causative agent of leprosy, is an obligate intracellular pathogen. M. leprae can infect a variety of cells in vivo, including epithelial cells, muscle cells, and Schwann cells, in addition to macrophages. The ligand-receptor interactions important in the attachment and ingestion of M. leprae by these nonmacrophage cells remains unknown. Fibronectin (FN) significantly enhances both attachment and ingestion of M. leprae by epithelial and Schwann cell lines. We cloned an M. leprae FN binding protein (FN attachment protein [FAP]) distinct from the 85ABC complex which has been shown previously to bind FN. The FAP open reading frame predicts a protein of 29.5 kDa with a 39-amino-acid signal peptide and was previously described as an antigen in leprosy patients. M. leprae FAP has homologies in M. vaccae, M. avium, and M. tuberculosis, as determined by Southern blotting and direct peptide analysis. Both anti-FAP antibodies and an Escherichia coli-expressed recombinant protein significantly blocked M. leprae attachment and internalization by T-24, an epithelial cell line, and JS1, a Schwann cell line. These data suggest that FN can be a bridging opsonic ligand for attachment of mycobacteria to nonphagocytes and that FAP plays an important role in this process. This may be an important step in the initiation of M. leprae infection in vivo.

Adhesins, Bacterial↗