scholarly journals Studies of Schwann cell proliferation. I. An analysis in tissue culture of proliferation during development, Wallerian degeneration, and direct injury.

1980 ◽  
Vol 84 (3) ◽  
pp. 739-752 ◽  
Author(s):  
J L Salzer ◽  
R P Bunge
Keyword(s):  
Cell Proliferation ◽  
Tissue Culture ◽  
Schwann Cell ◽  
Schwann Cells ◽  
Wallerian Degeneration ◽  
Variable Response ◽  
Experimental Conditions ◽  
Fetal Rat ◽  
Direct Injury ◽  
Dividing Cells

In this paper the stimuli for and pattern of Schwann cell proliferation are defined under various experimental conditions. We used a tissue culture system in which fetal rat dorsal root ganglia, treated to eliminate contaminating fibroblasts (Wood, P., 1976, Brain Res. 115:361--375), appear to recapitulate many aspects of the developing peripheral nervous system. We observed that: (a) proliferation of Schwann cells on neurites is initially rapid, but, as each neurite becomes fully ensheathed, division slows considerably and is confined to the periphery of the outgrowth; (b) during the period of rapid proliferation, excision of the ganglion causes a rapid decay in the number of dividing cells; (c) excision of the ganglion from more established cultures in which there was little ongoing proliferation resulted in a small increase in labeling at the site of excision for all Schwann cells and a substantial increase in labeling for myelin-related cells with a peak labeling period at 4 d; (d) direct mechanical injury during Wallerian degeneration is mitogenic for Schwann cells; (e) a variety of potential mitogens failed to stimulate Schwann cell proliferation, and (f) replated cells have a slightly higher level of proliferation and show a small and variable response to the addition of cAMP.

scholarly journals SCHWANN CELL PROLIFERATION IN DEVELOPING MOUSE SCIATIC NERVE

1967 ◽  
Vol 34 (3) ◽  
pp. 735-743 ◽  
Author(s):  
A. K. Asbury
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Sciatic Nerve ◽  
Schwann Cell ◽  
Schwann Cells ◽  
Generation Time ◽  
Dividing Cells ◽  
Mitotic Figures ◽  
Relationship Of ◽  
The Relationship

Proliferation of Schwann cells in neonatal mouse sciatic nerve was studied radioautographically in 1-µ glycol methacrylate sections. 28 mice were injected with thymidine-3H, 4 µc/g, 48 hr after birth, and were killed serially over the next 4 days. For the cell cycle following injection, the generation time was approximately 24 hr as determined by grain-count halving data; the duration of synthesis phase was 8 hr as determined from a curve constructed from the per cent of mitotic figures containing label; and the labeling index was 9% at 2 hr after injection. With these estimates, the per cent of Schwann cells proliferating was calculated to be 27%. In addition, roughly 25% of dividing cells appeared to cease division during the cell cycle under study. The relationship of these findings to other events during maturation of nerve is discussed.

The influence of nerve fibres on Schwann cell migration investigated in tissue culture

1949 ◽  
Vol 136 (884) ◽  
pp. 448-460 ◽  
Keyword(s):  
Tissue Culture ◽  
Schwann Cell ◽  
Schwann Cells ◽  
Wallerian Degeneration ◽  
Total Cell ◽  
Tissue Cultures ◽  
Nerve Fibres ◽  
Total Cell Population ◽  
Schwann Cell Migration ◽  
Sciatic Nerves

A study of tissue cultures prepared from rabbit sciatic nerves was undertaken to determine the effect of reinnervation on the amount of cell outwandering from nerves undergoing Wallerian degeneration. For this purpose, 25 and 100 days before culturing, some nerves were completely severed and reinnervation prevented, while others were crushed, allowing rapid reinnervation. It was found that reinnervation profoundly diminished the amount of Schwann cell outwandering, in comparison with the outwandering from non-reinnervated nerves. This effect extended only a few cm. distally to the lesion when the nerve was cultured 25 days after interruption, but by 100 days extended much farther towards the periphery. In the region a few cm. distally to the lesion the intensity of the effect was little if at all in­creased by prolonging the period between operation and culture. The effect was confirmed in reinnervated nerves prepared by complete severance and subsequent suture. Reinnervation influences only the Schwann cells in this way; the outwandering of cells other than Schwann cells did not differ significantly between reinnervated and non-reinnervated nerves. The total cell population within the nerves, estimated from histological sections, is not detectably affected by reinnervation. The interpretation suggested is that a specific adhesion deveops between Schwann cells and nerve fibres, and this prevents the migration during tissue culture of a proportion of the Schwann cells.

Axonal signalling and the making of olfactory ensheathing cells: a hypothesis

2006 ◽  
Vol 2 (3) ◽  
pp. 217-224 ◽  
Author(s):  
KONSTANTIN WEWETZER ◽  
GUDRUN BRANDES
Keyword(s):  
Schwann Cell ◽  
Schwann Cells ◽  
Specific Interaction ◽  
Neurotrophin Receptor ◽  
Olfactory Ensheathing Cells ◽  
Experimental Conditions ◽  
Neural Repair ◽  
Ensheathing Cells

Olfactory ensheathing cells (OECs) are Schwann cell-like glial cells of the olfactory system that promote neural repair under experimental conditions. It is a matter of debate in how far OECs resemble Schwann cells and whether they possess specific properties. Although OECs have been characterized mainly with respect to their regenerative effects after transplantation, both their cellular identity and the regulating factors involved have remained vague. The aim of this article is to define OEC and Schwann-cell identity in molecular terms, and to discuss crucial factors that are involved in determination in vitro and in vivo. Distinct OEC features such as the down-regulation of the low affinity neurotrophin receptor p75NTR by neuronal contact are apparent in vivo under physiological conditions, whereas OECs acquire a Schwann cell-like phenotype and up-regulate p75NTR expression in vitro and following transplantation into the lesioned spinal cord. This might indicate that establishment of the OEC phenotype depends on specific axonal stimuli. In this review we hypothesize that OECs and Schwann cells possess malleable cellular phenotypes that acquire distinct features only upon specific interaction with their natural neuronal partner. This concept is consistent with previous findings in vitro and in vivo, and might be relevant for studies that use OECs and Schwann cells for nervous system repair.

scholarly journals Cerebellar granule cells contain a membrane mitogen for cultured Schwann cells.

1989 ◽  
Vol 108 (2) ◽  
pp. 607-611 ◽  
Author(s):  
P W Mason ◽  
J W Bigbee ◽  
G H DeVries
Keyword(s):  
Cell Proliferation ◽  
Schwann Cell ◽  
Schwann Cells ◽  
Cell Cultures ◽  
Granule Cell ◽  
Granule Cells ◽  
Cerebellar Granule Cells ◽  
Proteoglycan Synthesis ◽  
Cerebellar Granule ◽  
Mitogenic Signal

Proliferation of Schwann cells is one of the first events that occurs after contact with a growing axon. To further define the distribution and properties of this axonal mitogen, we have (a) cocultured cerebellar granule cells, which lack glial ensheathment in vivo with Schwann cells; and (b) exposed Schwann cell cultures to isolated granule cell membranes. Schwann cells cocultured with granule cells had a 30-fold increase in the labeling index over Schwann cells cultured alone, suggesting that the mitogen is located on the granule cell surface. Inhibition of granule cell proteoglycan synthesis caused a decrease in the granule cells' ability to stimulate Schwann cell proliferation. Membranes isolated from cerebellar granule cells when added to Schwann cell cultures caused a 45-fold stimulation in [3H]thymidine incorporation. The granule cell mitogenic signal was heat and trypsin sensitive and did not require lysosomal processing by Schwann cells to elicit its proliferative effect. The ability of granule cells and their isolated membranes to stimulate Schwann cell proliferation suggests that the mitogenic signal for Schwann cells is a ubiquitous factor present on all axons regardless of their ultimate state of glial ensheathment.

scholarly journals Calcitonin gene-related peptide promotes Schwann cell proliferation.

1995 ◽  
Vol 129 (3) ◽  
pp. 789-796 ◽  
Author(s):  
L Cheng ◽  
M Khan ◽  
A W Mudge
Keyword(s):  
Cell Proliferation ◽  
Schwann Cell ◽  
Schwann Cells ◽  
Neutral Endopeptidase ◽  
Calcitonin Gene Related Peptide ◽  
Intracellular Camp ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Glial Growth Factor

Schwann cells in culture divide in response to defined mitogens such as PDGF and glial growth factor (GGF), but proliferation is greatly enhanced if agents such as forskolin, which increases Schwann cell intracellular cAMP, are added at the same time as PDGF or GGF (Davis, J. B., and P. Stroobant. 1990. J. Cell Biol. 110:1353-1360). The effect of forskolin is probably due to an increase in numbers of PDGF receptors (Weinmaster, G., and G. Lemke. 1990. EMBO (Eur. Mol. Biol. Organ.) J. 9:915-920. Neuropeptides and beta-adrenergic agonists have been reported to have no effect on potentiating the mitogenic response of either PDGF or GGF. We show that the neuropeptide calcitonin gene-related peptide (CGRP) increases Schwann cell cAMP levels, but the cells rapidly desensitize. We therefore stimulated the cells in pulsatile fashion to partly overcome the effects of desensitization and show that CGRP can synergize with PDGF to stimulate Schwann cell proliferation, and that CGRP is as effective as forskolin in the pulsatile regime. CGRP is a good substrate for the neutral endopeptidase 24.11. Schwann cells in vivo have this protease on their surface, so the action of CGRP could be terminated by this enzyme and desensitization prevented. We therefore suggest that CGRP may play an important role in stimulating Schwann cell proliferation by regulating the response of mitogenic factors such as PDGF.

scholarly journals Jab1 regulates Schwann cell proliferation and axonal sorting through p27

2013 ◽  
Vol 211 (1) ◽  
pp. 29-43 ◽  
Author(s):  
Emanuela Porrello ◽  
Cristina Rivellini ◽  
Giorgia Dina ◽  
Daniela Triolo ◽  
Ubaldo Del Carro ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Schwann Cell ◽  
Schwann Cells ◽  
Cell Cycle Progression ◽  
Cell Number ◽  
Cycle Progression ◽  
Neuregulin 1 ◽  
Regulatory Molecule ◽  
Axonal Sorting

Axonal sorting is a crucial event in nerve formation and requires proper Schwann cell proliferation, differentiation, and contact with axons. Any defect in axonal sorting results in dysmyelinating peripheral neuropathies. Evidence from mouse models shows that axonal sorting is regulated by laminin211– and, possibly, neuregulin 1 (Nrg1)–derived signals. However, how these signals are integrated in Schwann cells is largely unknown. We now report that the nuclear Jun activation domain–binding protein 1 (Jab1) may transduce laminin211 signals to regulate Schwann cell number and differentiation during axonal sorting. Mice with inactivation of Jab1 in Schwann cells develop a dysmyelinating neuropathy with axonal sorting defects. Loss of Jab1 increases p27 levels in Schwann cells, which causes defective cell cycle progression and aberrant differentiation. Genetic down-regulation of p27 levels in Jab1-null mice restores Schwann cell number, differentiation, and axonal sorting and rescues the dysmyelinating neuropathy. Thus, Jab1 constitutes a regulatory molecule that integrates laminin211 signals in Schwann cells to govern cell cycle, cell number, and differentiation. Finally, Jab1 may constitute a key molecule in the pathogenesis of dysmyelinating neuropathies.

Schwann Cell Reactions in Acute and Chronic Segmental Demyelinating Neuropathies

1968 ◽  
Vol 26 ◽  
pp. 108-109
Author(s):  
Roy O. Weller
Keyword(s):  
Schwann Cell ◽  
Peripheral Nerve ◽  
Schwann Cells ◽  
Myelin Sheath ◽  
Wallerian Degeneration ◽  
Demyelinating Disease ◽  
Segmental Demyelination ◽  
Recovery Stage ◽  
Myelin Sheaths ◽  
Demyelinating Neuropathies

The length of axon that each Schwann cell myelinates in a normal peripheral nerve is approximately proportional to the diameter of the axon and the thickness of the myelin sheath produced. When segmental demyelination occurs, individual segments, represented by the length of axon covered by one Schwann cell, lose their myelin sheaths but the axons are preserved. This differs from Wallerian degeneration where myelin destruction occurs along the length of a nerve fibre following death of the axon.In experimental diphtheritic neuropathy, an acute segmental demyelinating disease, lysosomes accumulate within the Schwann cells prior to disruption of the myelin sheath; furthermore, the site of initial myelin breakdown appears to be closely related to the collections of lysosomes. The Schwann cell starts to form a new myelin sheath around the axon probably within a few hours of the destruction of the original myelin sheath, and while the latter is being catabolised within lysosomal vacuoles This stage of remyelination follows a similar course to primary myelination, so that the recovery stage is characterised by normal axons with either no myelin, or surrounded by sheaths that are very thin relative to the diameter of the axon.

scholarly journals Neuron Regeneration and Proliferation Effects of Danshen and Tanshinone IIA

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Jui-Lung Shen ◽  
Yueh-Sheng Chen ◽  
Jing-Ying Lin ◽  
Yun-Chen Tien ◽  
Wen-Huang Peng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Schwann Cell ◽  
Schwann Cells ◽  
Map Kinases ◽  
Mapk Signaling ◽  
Tanshinone Iia ◽  
Dependent Manner ◽  
Neuron Regeneration

This study evaluates the proliferative effects of danshen and its monomer extract, tanshinone IIA, on Schwann cell proliferation. A piece of silicone rubber was guided across a 15-mm gap in the sciatic nerve of a rat. This nerve gap was then filled with different concentrations of danshen (0–100 mg/mL). The results showed that danshen increased the expressions of uPA, cyclin D1, E and ERK, JNK, and P38 MAP kinases via the FGF-2 signaling pathway in a dose-dependent manner. RSC96, Schwann cells were also administered with danshen (0, 20, 40, 60, 80, and 100 μg/mL) and tanshinone IIA (0, 2, 4, 6, 8, and 10 μg/mL). In lower concentrations, danshen and tanshinone IIA exhibited an apparent effect on Schwann cells. Similar effects were also demonstrated in the FGF-2-uPA regulating cascade and cell cycle proliferative protein results. Schwann cell migration was elevated as well. We used MAPK-signaling chemical inhibitors and identified the proliferative effects of danshen and tanshinone IIA as MAPK-signaling dependent. The results from thein vitrosystems indicate that danshen and tanshinone IIA can be used to induce Schwann cell proliferation, andin vivoresults potentially suggest that danshen and tanshinone IIA might enhance neuron regeneration.

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