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

Development ◽  
1990 ◽  
Vol 109 (1) ◽  
pp. 91-103 ◽  
Author(s):  
K.R. Jessen ◽  
L. Morgan ◽  
H.J. Stewart ◽  
R. Mirsky
Keyword(s):  
Sciatic Nerve ◽  
Schwann Cell ◽  
Schwann Cells ◽  
Cell Signalling ◽  
Surface Proteins ◽  
Developmental Changes ◽  
Rat Sciatic Nerve ◽  
Ngf Receptor ◽  
Cultured Schwann Cells ◽  
Do So

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.

scholarly journals Enhanced synthesis of brain-derived neurotrophic factor in the lesioned peripheral nerve: different mechanisms are responsible for the regulation of BDNF and NGF mRNA.

1992 ◽  
Vol 119 (1) ◽  
pp. 45-54 ◽  
Author(s):  
M Meyer ◽  
I Matsuoka ◽  
C Wetmore ◽  
L Olson ◽  
H Thoenen
Keyword(s):  
Sciatic Nerve ◽  
Schwann Cells ◽  
Neurotrophic Factor ◽  
Time Course ◽  
Interleukin 1 ◽  
Brain Derived Neurotrophic Factor ◽  
Mrna Levels ◽  
Bdnf Mrna ◽  
Rat Sciatic Nerve ◽  
Cultured Schwann Cells

Nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) are molecules which regulate the development and maintenance of specific functions in different populations of peripheral and central neurons, amongst them sensory neurons of neural crest and placode origin. Under physiological conditions NGF is synthesized by peripheral target tissues, whereas BDNF synthesis is highest in the CNS. This situation changes dramatically after lesion of peripheral nerves. As previously shown, there is a marked rapid increase in NGF mRNA in the nonneuronal cells of the damaged nerve. The prolonged elevation of NGF mRNA levels is related to the immigration of activated macrophages, interleukin-1 being the most essential mediator of this effect. Here we show that transsection of the rat sciatic nerve also leads to a very marked increase in BDNF mRNA, the final levels being even ten times higher than those of NGF mRNA. However, the time-course and spatial pattern of BDNF mRNA expression are distinctly different. There is a continuous slow increase of BDNF mRNA starting after day 3 post-lesion and reaching maximal levels 3-4 wk later. These distinct differences suggest different mechanisms of regulation of NGF and BDNF synthesis in non-neuronal cells of the nerve. This was substantiated by the demonstration of differential regulation of these mRNAs in organ culture of rat sciatic nerve and Schwann cell culture. Furthermore, using bioassays and specific antibodies we showed that cultured Schwann cells are a rich source of BDNF- and ciliary neurotrophic factor (CNTF)-like neurotrophic activity in addition to NGF. Antisera raised against a BDNF-peptide demonstrated BDNF-immunoreactivity in pure cultured Schwann cells, but not in fibroblasts derived from sciatic nerve.

scholarly journals Betacellulin regulates peripheral nerve regeneration by affecting Schwann cell migration and axon elongation

2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Yaxian Wang ◽  
Fuchao Zhang ◽  
Yunsong Zhang ◽  
Qi Shan ◽  
Wei Liu ◽  
...  
Keyword(s):  
Cell Migration ◽  
Sciatic Nerve ◽  
Schwann Cell ◽  
Peripheral Nerve ◽  
Nerve Regeneration ◽  
Schwann Cells ◽  
Nerve Injury ◽  
Axon Elongation ◽  
Rat Sciatic Nerve ◽  
Schwann Cell Migration

Abstract Background Growth factors execute essential biological functions and affect various physiological and pathological processes, including peripheral nerve repair and regeneration. Our previous sequencing data showed that the mRNA coding for betacellulin (Btc), an epidermal growth factor protein family member, was up-regulated in rat sciatic nerve segment after nerve injury, implying the potential involvement of Btc during peripheral nerve regeneration. Methods Expression of Btc was examined in Schwann cells by immunostaining. The function of Btc in regulating Schwann cells was investigated by transfecting cultured cells with siRNA segment against Btc or treating cells with Btc recombinant protein. The influence of Schwann cell-secreted Btc on neurons was determined using a co-culture assay. The in vivo effects of Btc on Schwann cell migration and axon elongation after rat sciatic nerve injury were further evaluated. Results Immunostaining images and ELISA outcomes indicated that Btc was present in and secreted by Schwann cells. Transwell migration and wound healing observations showed that transfection with siRNA against Btc impeded Schwann cell migration while application of exogenous Btc advanced Schwann cell migration. Besides the regulating effect on Schwann cell phenotype, Btc secreted by Schwann cells influenced neuron behavior and increased neurite length. In vivo evidence supported the promoting role of Btc in nerve regeneration after both rat sciatic nerve crush injury and transection injury. Conclusion Our findings demonstrate the essential roles of Btc on Schwann cell migration and axon elongation and imply the potential application of Btc as a regenerative strategy for treating peripheral nerve injury.

Regulation of neurofibromin expression in rat sciatic nerve and cultured Schwann cells

Glia ◽  
1995 ◽  
Vol 15 (1) ◽  
pp. 22-32 ◽  
Author(s):  
Lawrence Wrabetz ◽  
Maria Laura Feltri ◽  
Haesun Kim ◽  
Maryellen Daston ◽  
John Kamholz ◽  
...  
Keyword(s):  
Sciatic Nerve ◽  
Schwann Cells ◽  
Rat Sciatic Nerve ◽  
Cultured Schwann Cells

scholarly journals Identification of a lipid-anchored heparan sulfate proteoglycan in Schwann cells.

1990 ◽  
Vol 111 (5) ◽  
pp. 2053-2062 ◽  
Author(s):  
D J Carey ◽  
R C Stahl
Keyword(s):  
Sciatic Nerve ◽  
Schwann Cell ◽  
Cell Surface ◽  
Heparan Sulfate ◽  
Schwann Cells ◽  
Phytic Acid ◽  
Core Protein ◽  
Peripheral Cell ◽  
Rat Sciatic Nerve ◽  
Sds Page

Schwann cells synthesize both hydrophobic and peripheral cell surface heparan sulfate proteoglycans (HSPGs). Previous analysis of the kinetics of radiolabeling suggested the peripheral HSPGs are derived from the membrane-anchored forms (Carey, D., and D. Evans. 1989. J. Cell Biol. 108:1891-1897). Peripheral cell surface HSPGs were purified from phytic acid extracts of cultured neonatal rat sciatic nerve Schwann cells by anion exchange, gel filtration, and laminin-affinity chromatography. Approximately 250 micrograms of HSPG protein was obtained from 2 X 10(9) cells with an estimated recovery of 23% and an overall purification of approximately 2000-fold. SDS-PAGE analysis indicated the absence of non-HSPG proteins in the purified material. Analysis of heparinase digestion products revealed the presence of at least six core protein species ranging in molecular weight from 57,000 to 185,000. The purified HSPGs were used to produce polyclonal antisera in rabbits. The antisera immunoprecipitated a subpopulation of 35SO4-labeled HSPGs that were released from Schwann cells by incubation in medium containing phosphatidylinositol-specific phospholipase C (PI-PLC); smaller amounts of immunoprecipated HSPGs were also present in phytic acid extracts. In the presence of excess unlabeled PI-PLC-released proteins, immunoprecipitation of phytic acid-solubilized HSPGs was inhibited. SDS-PAGE analysis of proteins immunoprecipitated from extracts of [35S]methionine labeled Schwann cells demonstrated that the antisera precipitated an HSPG species that was present in the pool of proteins released by PI-PLC, with smaller amounts present in phytic acid extracts. Nitrous acid degradation of the immunoprecipitated proteins produced a single 67,000-Mr core protein. When used for indirect immunofluorescence labeling, the antisera stained the external surface of cultured Schwann cells. Preincubation of the cultures in medium containing PI-PLC but not phytic acid significantly reduced the cell surface staining. The antisera stained the outer ring of Schwann cell membrane in sections of adult rat sciatic nerve but did not stain myelin or axonal membranes. This localization suggests the HSPG may play a role in binding the Schwann cell plasma membrane to the adjacent basement membrane surrounding the individual axon-Schwann cell units.

scholarly journals Developmental changes in myelin-induced proliferation of cultured Schwann cells.

1987 ◽  
Vol 104 (3) ◽  
pp. 655-660 ◽  
Author(s):  
J E Yoshino ◽  
P W Mason ◽  
G H DeVries
Keyword(s):  
Cell Proliferation ◽  
Schwann Cell ◽  
Myelin Basic Protein ◽  
Schwann Cells ◽  
Basic Protein ◽  
Small Population ◽  
Developmental Changes ◽  
Cultured Schwann Cells

Schwann cell proliferation induced by a myelin-enriched fraction was examined in vitro. Although nearly all the Schwann cells contained material that was recognized by antisera to myelin basic protein after 24 h, only 1% of the cells were synthesizing DNA. 72 h after the addition of the mitogen a maximum of 10% of the cells incorporated [3H]thymidine. If the cultures were treated with the myelin-enriched fraction for 24 h and then washed, the number of proliferating Schwann cells decreased by 75% when compared with those cells that were incubated with the mitogen continuously. When Schwann cells were labeled with [14C]thymidine followed by a pulse of [3H]thymidine 24 h later, every Schwann cell labeled with [3H]thymidine was also labeled with [14C]thymidine. Although almost every Schwann cell can metabolize the myelin membranes within 24 h of exposure, a small population of cell initially utilizes the myelin as a mitogen, and this population continues to divide only if myelin is present in the extracellular media. The percentage of the Schwann cells that initially recognize the myelin-enriched fraction as a mitogen is dependent upon the age of the animal from which the cells were prepared.

Spontaneous immortalisation of Schwann cells in culture: short-term cultured Schwann cells secrete growth inhibitory activity

Development ◽  
1991 ◽  
Vol 112 (1) ◽  
pp. 33-42
Author(s):  
P.A. Eccleston ◽  
R. Mirsky ◽  
K.R. Jessen
Keyword(s):  
Growth Factor ◽  
Schwann Cell ◽  
Dna Synthesis ◽  
Schwann Cells ◽  
Inhibitory Activity ◽  
Short Term ◽  
Growth Inhibitory ◽  
Growth Inhibitory Activity ◽  
Cultured Schwann Cells

In the developing peripheral nerve, Schwann cells proliferate rapidly and then become quiescent, an essential step in control of Schwann cell differentiation. Cell proliferation is controlled by growth factors that can exert positive or inhibitory influences on DNA synthesis. It has been well established that neonatal Schwann cells divide very slowly in culture when separated from neurons but here we show that when culture was continued for several months some cells began to proliferate rapidly and non-clonal lines of immortalised Schwann cells were established which could be passaged for over two years. These cells had a similar molecular phenotype to short-term cultured Schwann cells, except that they expressed intracellular and cell surface fibronectin. The difference in proliferation rates between short- and long-term cultured Schwann cells appeared to be due in part to the secretion by short-term cultured Schwann cells of growth inhibitory activity since DNA synthesis of long-term, immortalised Schwann cells was inhibited by conditioned medium from short-term cultures. This conditioned medium also inhibited DNA synthesis in short-term Schwann cells stimulated to divide by glial growth factor or elevation of intracellular cAMP. The growth inhibitory activity was not detected in the medium of long-term immortalised Schwann cells, epineurial fibroblasts, a Schwannoma (33B), astrocytes or a fibroblast-like cell-line (3T3) and it did not inhibit serum-induced DNA synthesis in epineurial fibroblasts, 33B cells or 3T3 cells. The activity was apparently distinct from transforming growth factor-beta, activin, IL6, epidermal growth factor, atrial natriuretic peptide and gamma-interferon and was heat and acid stable, resistant to collagenase and destroyed by trypsin treatment. We raise the possibility that loss of an inhibitory autocrine loop may contribute to the rapid proliferation of long-term cultured Schwann cells and that an autocrine growth inhibitor may have a role in the cessation of Schwann cell division that precedes differentiation in peripheral nerve development.

scholarly journals S100ß and fibroblast growth factor-2 are present in cultured Schwann cells and may exert paracrine actions on the peripheral nerve injury

2008 ◽  
Vol 23 (6) ◽  
pp. 555-560 ◽  
Author(s):  
Tatiana Duobles ◽  
Thais de Sousa Lima ◽  
Beatriz de Freitas Azevedo Levy ◽  
Gerson Chadi
Keyword(s):  
Growth Factor ◽  
Sciatic Nerve ◽  
Fibroblast Growth Factor ◽  
Schwann Cells ◽  
Nerve Injury ◽  
Satellite Cells ◽  
Peripheral Nerves ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Cultured Schwann Cells

PURPOSE: The neurotrophic factor fibroblast growth factor-2 (FGF-2, bFGF) and Ca++ binding protein S100ß are expressed by the Schwann cells of the peripheral nerves and by the satellite cells of the dorsal root ganglia (DRG). Recent studies have pointed out the importance of the molecules in the paracrine mechanisms related to neuronal maintenance and plasticity of lesioned motor and sensory peripheral neurons. Moreover, cultured Schwann cells have been employed experimentally in the treatment of central nervous system lesions, in special the spinal cord injury, a procedure that triggers an enhanced sensorymotor function. Those cells have been proposed to repair long gap nerve injury. METHODS: Here we used double labeling immunohistochemistry and Western blot to better characterize in vitro and in vivo the presence of the proteins in the Schwann cells and in the satellite cells of the DRG as well as their regulation in those cells after a crush of the rat sciatic nerve. RESULTS: FGF-2 and S100ß are present in the Schwann cells of the sciatic nerve and in the satellite cells of the DRG. S100ß positive satellite cells showed increased size of the axotomized DRG and possessed elevated amount of FGF-2 immunoreactivity. Reactive satellite cells with increased FGF-2 labeling formed a ring-like structure surrounding DRG neuronal cell bodies.Reactive S100ß positive Schwann cells of proximal stump of axotomized sciatic nerve also expressed higher amounts of FGF-2. CONCLUSION: Reactive peripheral glial cells synthesizing FGF-2 and S100ß may be important in wound repair and restorative events in the lesioned peripheral nerves.

The effects of embryonic retinal neurons on neural crest cell differentiation into Schwann cells

Development ◽  
1990 ◽  
Vol 109 (4) ◽  
pp. 925-934 ◽  
Author(s):  
L.C. Smith-Thomas ◽  
A.R. Johnson ◽  
J.W. Fawcett
Keyword(s):  
Schwann Cell ◽  
Neural Crest ◽  
Schwann Cells ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Cell Types ◽  
Cell Markers ◽  
Ngf Receptor ◽  
S 100 ◽  
The Many

Amongst the many cell types that differentiate from migratory neural crest cells are the Schwann cells of the peripheral nervous system. While it has been demonstrated that Schwann cells will not fully differentiate unless in contact with neurons, the factors that cause neural crest cells to enter the differentiative pathway that leads to Schwann cells are unknown. In a previous paper (Development 105: 251, 1989), we have demonstrated that a proportion of morphologically undifferentiated neural crest cells express the Schwann cell markers 217c and NGF receptor, and later, as they acquire the bipolar morphology typical of Schwann cells in culture, express S-100 and laminin. In the present study, we have grown axons from embryonic retina on neural crest cultures to see whether this has an effect on the differentiation of neural crest cells into Schwann cells. After 4 to 6 days of co-culture, many more cells had acquired bipolar morphology and S-100 staining than in controls with no retinal explant, and most of these cells were within 200 microns of an axon, though not necessarily in contact with axons. However, the number of cells expressing the earliest Schwann cell markers 217c and NGF receptor was not affected by the presence of axons. We conclude that axons produce a factor, which is probably diffusible, and which makes immature Schwann cells differentiate. The factor does not, however, influence the entry of neural crest cells into the earliest stages of the Schwann cell differentiative pathway.

A comparison of the release of a vasoactive-intestinal-peptide-like peptide and acetylcholine in the giant axon-Schwann cell preparation of the tropical squid Sepioteuthis sepioidea

1999 ◽  
Vol 202 (4) ◽  
pp. 417-428
Author(s):  
P.D. Evans ◽  
V. Reale ◽  
R.M. Merzon ◽  
J. Villegas
Keyword(s):  
Schwann Cell ◽  
Vasoactive Intestinal Peptide ◽  
Schwann Cells ◽  
Recovery Time ◽  
Cell Signalling ◽  
Giant Axon ◽  
Direct Application ◽  
Cell Preparation ◽  
Signalling Molecule ◽  
Release Of Acetylcholine

A vasoactive intestinal peptide (VIP)-like peptide is released by axonal stimulation in the giant axon-Schwann cell preparation from the tropical squid Sepioteuthis sepioidea. It is also released by direct application of l-glutamate, the giant axon-Schwann cell signalling molecule in this preparation. The release of the peptide parallels the release of acetylcholine from the Schwann cells themselves in this preparation in a number of different ways. The release of both acetylcholine and the VIP-like peptide have the same threshold (between 2×10(−10) and 5×10(−10)mol l-1) for l-glutamate application and the same recovery time after inhibition of release by exposure of the preparation to a prolonged pulse of l-glutamate. A prolonged l-glutamate pulse of 10(−8)mol l-1 releases both substances for as long as the pulse is applied to the preparation, whereas a prolonged pulse of 10(−9)mol l-1 l-glutamate releases acetylcholine in the same way but releases the VIP-like peptide only transiently. The VIP-like peptide is likely to be co-released with acetylcholine from the Schwann cells.

Schwann-Cell Proliferation in Muscle-Vein Combined Conduits for Bridging Rat Sciatic Nerve Defects

2003 ◽  
Vol 19 (2) ◽  
pp. 119-123 ◽  
Author(s):  
S. Geuna ◽  
S. Raimondo ◽  
S. Nicolino ◽  
E. Boux ◽  
M. Fornaro ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Sciatic Nerve ◽  
Schwann Cell ◽  
Rat Sciatic Nerve
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