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PubMed1993

Neuron-Schwann cell signals are conserved across species: purification and characterization of embryonic chicken Schwann cells.

A monoclonal antibody, 1E8, which recognizes the peripheral myelin protein, P0, specific for chicken Schwann cells and their precursors (Bhattacharyya et al., Neuron 7:831-844, 1991), was used to immunoselect Schwann cells from embryonic day 14 (E14) chicken sciatic nerve. When cultured, these immunoselected cells displayed properties characteristic of perinatal rodent Schwann cells, including S100-immunoreactivity and O4 antigen-immunoreactivity. In addition, the purified chicken Schwann cells divided slowly when cultured alone, but when co-cultured with chicken or rat sensory neurons, they bound to axons and proliferated. Proliferation was also stimulated by the addition of bovine brain membrane extracts or chicken brain membranes. The 1E8 monoclonal antibody was also used to test the effect of axonal contact on P0 expression. Chicken Schwann cells purified using the 1E8 monoclonal antibody gradually lost P0 when cultured alone. These cells remained 1E8-negative even after prolonged co-culture with embryonic rat dorsal root ganglion neurons or chicken sensory ganglia. These results demonstrate that chicken Schwann cells behave like rodent Schwann cells in their expression of specific antigens, interactions with axons, and regulation of P0 expression. In addition, chicken Schwann cells respond to neuronal signals from the rat and cow, illustrating the cross-species conservation of these signals.

Animals↗

PubMed1985

Adhesion of axolemmal fragments to Schwann cells: a signal- and target-specific process closely linked to axolemmal induction of Schwann cell mitosis.

Radioiodinated rat CNS axolemmal fragments adhered to cultured rat Schwann cells by a time-, temperature-, and concentration-dependent process independent of extracellular ionized calcium. Adhesion showed target and signal specificity; axolemmal fragments adhered to endoneurial or dermal fibroblasts to a much lesser extent than to Schwann cells, and plasma membrane fragments from skeletal muscle, erythrocytes, or PNS myelin adhered to Schwann cells to a lesser extent than did axolemmal fragments. Brief trypsinization removed 94 to 97% of bound radioactivity from Schwann cells previously incubated with 125I-axolemmal fragments for up to 24 hr, indicating that adhesion was largely a surface phenomenon rather than the result of rapid internalization of axolemmal fragments by the Schwann cells. When adhesion was compared to the axolemmal mitogenic response of Schwann cells, the concentration of axolemmal fragments yielding half-maximal adhesion was the same as the concentration producing half-maximal stimulation of Schwann cell mitosis. Trypsin digestion, homogenization, or heating of axolemmal fragments before application to cultured Schwann cells diminished adhesion and axolemmal fragment-induced stimulation of Schwann cell mitosis in a parallel fashion. Whereas adhesion of axolemmal fragments to the surfaces of the cultured Schwann cells reached completion within 4 hr in this assay system, induction of Schwann cell mitosis by the fragments required contact with Schwann cells for a minimum of 6 to 8 hr and reached a maximum when the axolemmal fragments had adhered to the Schwann cells for 24 hr or more.

Animals↗

PubMed1993

Induction of neuronal morphology in adrenal chromaffin cells cocultured with denervated Schwann cells.

We have studied the interactions of adrenal chromaffin and Schwann cells in a coculture system to observe whether denervated Schwann cells induce and support chromaffin cell differentiation in a manner analogous to nerve growth factor (NGF). Schwann cells induce both the accumulation of intense clumps of cocultured chromaffin cells on their surfaces and intense neurite outgrowth. This interaction is not blocked by antibodies to NGF or laminin. Conditioned medium from Schwann cell cultures fosters neurite outgrowth in chromaffin cells in a fashion qualitatively similar to NGF. Our data indicate that denervated Schwann cells exert a profound aggregating and differentiating effect upon chromaffin cells, inducing the expression of a neuronal phenotype via a predominantly NGF-independent mechanism.

Adrenal Glands↗

PubMed1996

Embryonic development of Schwann cells: multiple roles for neuregulins along the pathway.

During the past few years important advances have been realized in the understanding of the molecular and cellular mechanisms operating in the differentiation of Schwann cells from neural crest cells. In particular the development of in vitro culture systems has allowed the analysis of commitment to the Schwann cell lineage, identification of an intermediate between the neural crest cell and the Schwann cell, and initial analysis of the factors controlling determination and differentiation processes. These studies point in particular to major roles for neuregulins which appear to be involved in the control of cell survival, proliferation, and differentiation, as well as of gene expression at different levels of the pathway.

Animals↗

PubMed1990

Schwann-cell differentiation in clonal cultures of the neural crest, as evidenced by the anti-Schwann cell myelin protein monoclonal antibody.

In the vertebrate embryo, Schwann cells lining the peripheral nerves originate from the neural crest (NC), a structure that also gives rise to ganglion satellite cells, most of the neurons of the peripheral nervous system, melanocytes, and part of the cranial mesenchyme. We have studied the emergence of the Schwann cell lineage in vitro in clonal cultures of quail mesencephalic NC cells by using the Schwann cell myelin protein antigen as an early and specific marker for myelinating and nonmyelinating cells. After 13-16 days in culture, numerous clones contained Schwann cell myelin protein-positive cells, sometimes isolated and sometimes associated with other NC-derived cell types. Detailed phenotypic analysis of the clones allowed us to infer the presence of differently committed Schwann-cell ancestors in the NC during the migration stage. In particular, we found evidence for the existence of a bipotent precursor of Schwann cells and nonneuronal satellite cells; a common precursor of neurons, satellite cells, and Schwann cells; and a pluripotent precursor of Schwann cells, satellite cells, neurons, and melanocytes. These founder cell types coexist in the NC with a committed Schwann cell progenitor of high-proliferative potential that differentiates in vitro in the absence of other peripheral cells and axons.

Animals↗

PubMedDate not supplied

The effect of cell numbers on Schwann cell radioimmunoassay for serum cytotoxicity.

Immune cytotoxic effects on cultured Schwann cells can be monitored by a 51Cr release cytotoxicity assay. This paper presents the results of experiments using different cell numbers in the assay and a revision of the method for calculating the % specific release of 51Cr. The results give a more reliable and quantitative method for distinguishing between different sera.

Cell Count↗

PubMed1992

Myelination of two axons by a single Schwann cell.

A Schwann cell can form only one internode of myelin around an axon. However, we observed the formation by a single Schwann cell of myelin around two axons of different diameters in the sural nerve of a 45-year-old man with mononeuritis multiplex. Schwann cell processes spiraled in the same direction around each axon, forming mesaxons. The findings in this case appear to be an undescribed type of aberrant myelination.

Axons↗

PubMed1999

[Rescue of motoneuron from brachial plexus nerve root avulsion induced cell death by Schwann cell derived neurotrophic factor].

OBJECTIVE: To study the protective effects of Schwann cell derived neurotrophic factor (SDNF) on motoneurons of spinal anterior horn from spinal root avulsion induced cell death. METHODS: Twenty SD rats were made the animal model of C6.7 spinal root avulsion induced motoneuron degeneration, and SDNF was applied at the lesion site of spinal cord once a week. After three weeks, the C6.7 spinal region was dissected out for motoneuron count, morphological analysis and nitric oxide synthase (NOS) enzyme histochemistry. RESULTS: 68.6% motoneurons of spinal anterior horn death were occurred after 3 weeks following surgery, the size of survivors was significantly atrophy and NOS positive neurons increased. However, in animals which received SDNF treatment, the death of motoneurons was significantly decreased, the atrophy of surviving motoneurons was prevented, and expression of NOS was inhibited. CONCLUSION: SDNF can prevent the death of motoneurons following spinal root avulsion. Nitric oxide may play a role in these injury induced motoneuron death.

Animals↗

PubMed1984

PC12 cells as a source of neurite-derived cell surface mitogen, which stimulates Schwann cell division.

Primary cultures of rat dorsal root ganglion Schwann cells were used to assay the efficacy of PC12 cells in stimulating Schwann cell proliferation. Co-cultures of PC12 cells and Schwann cells assayed by [3H]thymidine labeling followed by autoradiography showed proliferation of Schwann cells only where contact occurred between PC12 neurites and Schwann cells. Membranes derived from PC12 cells were shown to have many characteristics similar to membranes derived from sensory neurons; both could mimic whole cells in stimulating Schwann cell division; both were inactivated by mild heat treatment and by trypsinization, and both elevated intracellular cyclic AMP concentrations in Schwann cells 16 h after addition of membranes. We conclude that PC12 cells will be a valuable source for the isolation of the neuronal cell surface component which controls proliferation of Schwann cells during development of the peripheral nervous system.

Animals↗

PubMed1995

Schwann cell responses to forskolin and cyclic AMP analogues: comparative study of mouse and rat Schwann cells.

Forskolin and cAMP analogues (8-bromo cAMP and dibutyryl cAMP) induced proliferation or surface galC expression, depending on the concentrations, in rat and mouse Schwann cells in vitro. However, rat Schwann cells required much higher concentrations of these agents than mouse Schwann cells in both proliferation and surface galC expression. The concentrations needed for cellular proliferation were 0.5 microM forskolin or 10 microM cAMP analogues in mice and 2.5 microM forskolin or 50 microM cAMP analogues in rats. Surface galC was expressed in mouse Schwann cells at concentrations of 10 microM forskolin or 100 microM cAMP analogues, while in rat Schwann cells, 50 microM forskolin or 500 microM cAMP analogues was needed for expression of surface galC. Rat Schwann cells transformed from an elongated spindle shape to flattened cells by the addition of these agents. However, mouse Schwann cells remained spindle shaped and their processes were apparently elongated at concentrations of more than 1.0 microM forskolin or 100 microM cAMP analogues. These results may reflect the differences in the cellular metabolism between mouse and rat cells. Moreover, the elongation of mouse Schwann cell processes appeared to be associated with surface galC expression, suggesting that elongation may be an initial signal for differentiation in mouse Schwann cells.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1997

Schwann cell differentiation in Charcot-Marie-Tooth disease type 1A (CMT1A): normal number of myelinating Schwann cells in young CMT1A patients and neural cell adhesion molecule expression in onion bulbs.

Charcot-Marie-Tooth disease type 1A (CMT1A) is a common hereditary demyelinating neuropathy caused by a duplication of the gene for the myelin protein PMP22, resulting in overexpression of PMP22 in young patients. Although genetically well defined, the pathogenesis of the hereditary demyelinating neuropathy CMT1A is still unclear. Homology of PMP22 cDNA to the growth arrest-specific gene gas3 and experiments in vitro showing decreased proliferation in PMP22-overexpressing Schwann cells suggest a role of PMP22 in Schwann cell differentiation. Furthermore, overexpression of PMP22 in fibroblasts induces programmed cell death. In this report we applied morphometrical methods using electron micrographs and immunohistochemistry to further characterise Schwann cells in CMT1A nerve biopsy samples from CMT1A patients. We show that the total number of PMP22-expressing Schwann cells, i.e. Schwann cells that are in a 1:1 relationship with axons, was not reduced in sural nerve biopsy samples from six young CMT1A patients. We excluded non-specific secondary Schwann cell proliferation. Thus, in young CMT1A patients with increased PMP22 overexpression there seems to be no evidence for altered initial Schwann cell proliferation in achieving a 1:1 relationship to axons prior to the process of de- and remyelination. Further, using electron microscopy we found no evidence for apoptosis of Schwann cells in CMT1A. However, we provide additional support for an abnormal Schwann cell phenotype in CMT1A by showing the expression of neural cell adhesion molecule immunoreactivity in onion bulbs. Thus, the role of PMP22 in cell growth and differentiation does not lead to an altered number of myelinating Schwann cells but to altered Schwann cell differentiation in CMT1A.

Cell Differentiation↗

PubMed1990

04 and A007-sulfatide antibodies bind to embryonic Schwann cells prior to the appearance of galactocerebroside; regulation of the antigen by axon-Schwann cell signals and cyclic AMP.

In the rat sciatic nerve, the relationship between Schwann cells, axons, the extracellular matrix and perineurial sheath cells undergoes extensive modification between embryo day 15 and the onset of myelination during the first postnatal day. Little is known about molecular changes in Schwann cells in this important prenatal period. In the present paper, we use immunofluorescence to study the prenatal development and postnatal regulation of the antigen(s) recognized by the 04 monoclonal antibody and a well-characterized rat monoclonal antibody to sulfatide, A007. We show that, in a series of immunochemical tests, the 04 antibody recognizes only sulfatide in neonatal and adult rat nerves. Both antibodies first bind to Schwann cells in the sciatic nerve at embryo day 16-17, and all Schwann cells bind both antibodies at birth. In the adult nerve, both nonmyelin-forming and myelin-forming cells are labelled with the antibodies. Schwann cells dissociated from embryo day 15 nerves and cultured in the absence of axons develop neither 04 nor A007 binding on schedule, and 04-positive and A007-positive Schwann cells from postnatal nerves lose the ability to bind these antibodies during the first few days in culture. Schwann cells in the distal stump of transected nerves also sharply down-regulate cell surface binding of 04. High numbers of 04-positive or A007-positive Schwann cells reappear in cultures treated with agents that mimic or elevate intracellular cAMP. We conclude that two anti-sulfatide antibodies 04 and A007, recognize an antigen, probably sulfatide, that appears very early in Schwann cell development (one to two days prior to galactocerebroside) but is nevertheless subject to upregulation by axonal contact or elevation of intracellular cAMP.

Animals↗

PubMed1994

Negative regulation of the P0 gene in Schwann cells: suppression of P0 mRNA and protein induction in cultured Schwann cells by FGF2 and TGF beta 1, TGF beta 2 and TGF beta 3.

During the development of peripheral nerves, Schwann cells are induced to form myelin sheaths round the larger axons. This process involves a complex series of events and the nature of the molecular signals that regulate and control myelin formation in Schwann cells is not well understood. Our previous experiments on rat Schwann cells in vitro, using serum-free defined medium, showed that a myelin-related protein phenotype could be induced in early postnatal Schwann cells in culture by elevation of intracellular cyclic AMP levels in the absence of growth factors, conditions under which the cells are not dividing. Cells with this phenotype expressed the major myelin glycoprotein P0 and expression of p75 NGF receptor, N-CAM, GFAP and A5E3 proteins was down-regulated. These changes are all characteristics associated with myelination in vivo. In contrast, when cyclic AMP levels were elevated in the presence of serum, suppression of cyclic AMP-induced differentiation resulted and DNA synthesis was induced. In this paper, we have used this model system and extended our analysis to explore the relationship between defined growth factors and suppression of myelination. We have used pure recombinant growth factors normally present in peripheral nerves, i.e. FGF1 and FGF2 and TGF beta 1, TGF beta 2, and TGF beta 3 and shown that, like serum, they can strongly suppress the forskolin-mediated induction of the P0 gene, both at the level of mRNA and protein synthesis. For both growth factor families, the suppression of P0 gene expression is dose-dependent and takes place in serum-starved cells that are mitotically quiescent. In the case of FGF2, however, even more complete suppression is obtained when the cells are simultaneously allowed to enter the cell cycle by inclusion of high concentrations of insulin in the culture medium. The present results raise the possibility that, in addition to the positive axonal signals that are usually envisaged to control the onset of myelination, growth factors present in the nerve may exert negative regulatory signals during development and thus help control the time of onset and the rate of myelination in peripheral nerves.

Animals↗

PubMed2006

Proteomic evaluation reveals that olfactory ensheathing cells but not Schwann cells express calponin.

Human clinical trials have begun worldwide that use olfactory ensheathing cells (OECs) to ameliorate the functional deficits following spinal cord injury. These trials have been initiated largely because numerous studies have reported that OECs transform into Schwann Cell (SC)-like cells that myelinate axons and support new growth in adult rats with spinal injury. This phenomenon is remarkable because OECs do not myelinate olfactory axons in their native environment. Furthermore, these myelinating OECs are morphologically identical to SCs, which can invade the spinal cord after injury. One factor that has contributed to a possible confusion in the identification of these cells is the lack of phenotypic markers to distinguish unequivocally between OECs and SCs. Such markers are required to first assess the degree of SC contamination in OEC cultures before intraspinal implantation, and then to accurately identify grafted OECs and invading SCs in the injured spinal cord. Using two-dimensional gel electrophoresis, we have identified calponin, an actin binding protein, as the first definitive phenotypic marker that distinguishes between OECs and SCs in vitro and in vivo. We have also provided ultrastructural evidence that calponin-immunopositive OECs do not transform into myelinating SC-like cells after intraspinal implantation. Rather, the grafted OECs retain their morphological and neurochemical features. These data yield new insight into the phenotypic characteristics of OECs, which together with invading SCs can enhance regeneration of the injured spinal cord.

Animals↗

PubMed1994

The Schwann cell precursor and its fate: a study of cell death and differentiation during gliogenesis in rat embryonic nerves.

We have characterized a cell, the Schwann cell precursor, that represents a distinct intermediate differentiation stage in the process by which Schwann cells are generated from neural crest cells. The Schwann cell precursor shows radical differences from Schwann cells which include death regulation, antigenic phenotype, pattern of cell-cell interaction, migratory behavior, and morphology. In the nerves of the rat hind limb, Schwann cells are irreversibly generated from these during a brief period, essentially embryonic days 15-17. We also provide evidence that the survival of Schwann cell precursors is regulated by neurons and identify basic fibroblast growth factor as a potential key regulator of apoptosis in Schwann cell precursors and of precursor to Schwann cell conversion. These findings have implications for our understanding of gliogenesis in the peripheral nervous system.

Animals↗

PubMed1981

Schwann cell and glial responses in beta, beta'-iminodipropionitrile intoxication. I. Schwann cell and oligodendrocyte ingrowths.

In rats continuously exposed to beta, beta'-iminodipropionitrile (DPN) for long periods, numerous Schwann cell and oligodendrocyte ingrowths extending into giant axonal swellings were found. These ingrowths, cytoplasmic processes of the Schwann cells and oligodendrocytes which deeply indented the axon, regularly arose from Schmidt-Lanterman clefts in the internodes. They dissected along an intra-axonal 'cleavage plane' which separated the giant axonal swellings into two compartments: an inner central channel of relatively normal axoplasm and an outer 'axoplasmic pad' comprised of circularly or spirally-arranged masses of neurofilaments. Multiple ingrowths often arose within a single internode, resulting in nearly complete segregation of the axoplasmic pad from the central channel over long distances. At the interface between the two axoplasmic compartments, internal myelin sheaths were occasionally found. The distinctive ingrowths found in this study appear to represent unusual responses of the Schwann cells and oligodendrocytes to the primary neurofilamentous axonal pathology produced by IDPN.

Animals↗

PubMed1990

Three markers of adult non-myelin-forming Schwann cells, 217c(Ran-1), A5E3 and GFAP: development and regulation by neuron-Schwann cell interactions.

Immunohistochemical methods are used to investigate in detail the development and regulation of three proteins (217c(Ran-1), A5E3 and GFAP) specifically associated with adult non-myelin-forming Schwann cells in the rat sciatic nerve, from embryo day 15 to maturity. 217c(Ran-1), which is probably the NGF-receptor, and A5E3 are expressed by the majority of cells in the nerve at embryo day 15 and by essentially all cells at embryo day 18. GFAP first appears at embryo day 18; this is an intrinsically programmed developmental event which occurs in cultured Schwann cells even in the absence of serum. Postnatally, the expression of 217c(Ran-1), A5E3 and GFAP is suppressed in cells that form myelin but retained in non-myelin-forming Schwann cells. Mature myelin-forming cells nevertheless maintain the potential to express all three proteins but will only do so if removed from contact with myelinated axons. In neuron-free cultures Schwann cells express all three proteins. This work, together with our previous observations on N-CAM, shows that removal of a diverse set of surface proteins and a change in intermediate filament expression is one of the major consequences of axon to Schwann cell signalling during myelination in the rat sciatic nerve. Unlike myelin-forming cells, adult non-myelin-forming Schwann cells remain very similar to embryonic and newborn cells with respect to expression of surface proteins, in contrast to the previously established developmental changes that occur in their surface lipids.

Animals↗

PubMed2006

ErbB2 signaling in Schwann cells is mostly dispensable for maintenance of myelinated peripheral nerves and proliferation of adult Schwann cells after injury.

Neuregulin/erbB signaling is critically required for survival and proliferation of Schwann cells as well as for establishing correct myelin thickness of peripheral nerves during development. In this study, we investigated whether erbB2 signaling in Schwann cells is also essential for the maintenance of myelinated peripheral nerves and for Schwann cell proliferation and survival after nerve injury. To this end, we used inducible Cre-loxP technology using a PLP-CreERT2 allele to ablate erbB2 in adult Schwann cells. ErbB2 expression was markedly reduced after induction of erbB2 gene disruption with no apparent effect on the maintenance of already established myelinated peripheral nerves. In contrast to development, Schwann cell proliferation and survival were not impaired in mutant animals after nerve injury, despite reduced levels of MAPK-P (phosphorylated mitogen-activated protein kinase) and cyclin D1. ErbB1 and erbB4 do not compensate for the loss of erbB2. We conclude that adult Schwann cells do not require major neuregulin signaling through erbB2 for proliferation and survival after nerve injury, in contrast to development and in cell culture.

Animals↗