Spontaneously immortalized Schwann cells from adult Fischer rat as a valuable tool for exploring neuron-Schwann cell interactions

2011 ◽  
Vol 89 (6) ◽  
pp. 898-908 ◽  
Author(s):  
Kazunori Sango ◽  
Hiroko Yanagisawa ◽  
Emiko Kawakami ◽  
Shizuka Takaku ◽  
Kyoko Ajiki ◽  
...  
Keyword(s):  
Schwann Cell ◽  
Schwann Cells ◽  
Cell Interactions ◽  
Immortalized Schwann Cells

Axon-Schwann cell interactions regulate the expression of c-jun in Schwann cells

1996 ◽  
Vol 43 (5) ◽  
pp. 511-525 ◽  
Author(s):  
M.E. Shy ◽  
Y. Shi ◽  
L. Wrabetz ◽  
J. Kamholz ◽  
S.S. Scherer
Keyword(s):  
Schwann Cell ◽  
Schwann Cells ◽  
Cell Interactions

scholarly journals The Collapsin Response Mediator Protein 5 Onconeural Protein Is Expressed in Schwann Cells Under Axonal Signals and Regulates Axon—Schwann Cell Interactions

2012 ◽  
Vol 71 (4) ◽  
pp. 298-311 ◽  
Author(s):  
Jean-Philippe Camdessanché ◽  
Karine Ferraud ◽  
Nadia Boutahar ◽  
François Lassabliére ◽  
Marie Mutter ◽  
...  
Keyword(s):  
Schwann Cell ◽  
Schwann Cells ◽  
Cell Interactions ◽  
Collapsin Response Mediator Protein ◽  
Mediator Protein

Spontaneously immortalized adult Fischer rat Schwann cells IFRS1 as a valuable tool for exploring neuron–Schwann cell interactions

2010 ◽  
Vol 68 ◽  
pp. e242
Author(s):  
Kazunori Sango ◽  
Kyoko Ajiki ◽  
Emiko Kawakami ◽  
Hiroko Yanagisawa ◽  
Shizuka Takaku ◽  
...  
Keyword(s):  
Schwann Cell ◽  
Schwann Cells ◽  
Cell Interactions

Expression of growth-associated protein-43 kD in Schwann cells is regulated by axon-Schwann cell interactions and cAMP

1994 ◽  
Vol 38 (5) ◽  
pp. 575-589 ◽  
Author(s):  
S. S. Scherer ◽  
Y.-T. Xu ◽  
D. Roling ◽  
L. Wrabetz ◽  
M. L. Feltri ◽  
...  
Keyword(s):  
Schwann Cell ◽  
Schwann Cells ◽  
Cell Interactions

scholarly journals Transforming growth factor-beta 1 regulates axon/Schwann cell interactions.

1995 ◽  
Vol 129 (2) ◽  
pp. 443-458 ◽  
Author(s):  
S Einheber ◽  
M J Hannocks ◽  
C N Metz ◽  
D B Rifkin ◽  
J L Salzer
Keyword(s):  
Schwann Cell ◽  
Schwann Cells ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Cell Interactions ◽  
Receptor Expression ◽  
Cell Phenotype ◽  
Beta Activity ◽  
Tgf Beta

We have investigated the potential regulatory role of TGF-beta in the interactions of neurons and Schwann cells using an in vitro myelinating system. Purified populations of neurons and Schwann cells, grown alone or in coculture, secrete readily detectable levels of the three mammalian isoforms of TGF-beta; in each case, virtually all of the TGF-beta activity detected is latent. Expression of TGF-beta 1, a major isoform produced by Schwann cells, is specifically and significantly downregulated as a result of axon/Schwann cell interactions. Treatment of Schwann cells or Schwann cell/neuron cocultures with TGF-beta 1, in turn, has dramatic effects on proliferation and differentiation. In the case of purified Schwann cells, treatment with TGF-beta 1 increases their proliferation, and it promotes a pre- or nonmyelinating Schwann cell phenotype characterized by increased NCAM expression, decreased NGF receptor expression, inhibition of the forskolin-mediated induction of the myelin protein P0, and induction of the Schwann cell transcription factor suppressed cAMP-inducible POU protein. Addition of TGF-beta 1 to the cocultures inhibits many of the effects of the axon on Schwann cells, antagonizing the proliferation induced by contact with neurons, and, strikingly, blocking myelination. Ultrastructural analysis of the treated cultures confirmed the complete inhibition of myelination and revealed only rudimentary ensheathment of axons. Associated defects of the Schwann cell basal lamina and reduced expression of laminin were also detected. These effects of TGF-beta 1 on Schwann cell differentiation are likely to be direct effects on the Schwann cells themselves which express high levels of TGF-beta 1 receptors when cocultured with neurons. The regulated expression of TGF-beta 1 and its effects on Schwann cells suggest that it may be an important autocrine and paracrine mediator of neuron/Schwann cell interactions. During development, TGF-beta 1 could serve as an inhibitor of Schwann cell proliferation and myelination, whereas after peripheral nerve injury, it may promote the transition of Schwann cells to a proliferating, nonmyelinating phenotype, and thereby enhance the regenerative response.

scholarly journals Mast cells can contribute to axon–glial dissociation and fibrosis in peripheral nerve

2007 ◽  
Vol 3 (3) ◽  
pp. 233-244 ◽  
Author(s):  
Kelly R. Monk ◽  
Jianqiang Wu ◽  
Jon P. Williams ◽  
Brenda A. Finney ◽  
Maureen E. Fitzgerald ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Schwann Cell ◽  
Peripheral Nerve ◽  
Schwann Cells ◽  
Cell Number ◽  
Cell Interactions ◽  
Disodium Cromoglycate ◽  
Collagen Deposition ◽  
Genetic Ablation

AbstractExpression of the human epidermal growth factor receptor (EGFR) in murine Schwann cells results in loss of axon–Schwann cell interactions and collagen deposition, modeling peripheral nerve response to injury and tumorigenesis. Mast cells infiltrate nerves in all three situations. We show that mast cells are present in normal mouse peripheral nerve beginning at 4 weeks of age, and that the number of mast-cells in EGFR+ nerves increases abruptly at 5–6 weeks of age as axons and Schwann cells dissociate. The increase in mast cell number is preceded and accompanied by elevated levels of mRNAs encoding the mast-cell chemoattractants Rantes, SCF and VEGF. Genetic ablation of mast cells and bone marrow reconstitution in W41 × EGFR+ mice indicate a role for mast cells in loss of axon−Schwann cell interactions and collagen deposition. Pharmacological stabilization of mast cells by disodium cromoglycate administration to EGFR+ mice also diminished loss of axon−Schwann cell interaction. Together these three lines of evidence support the hypothesis that mast cells can contribute to alterations in peripheral nerves.

scholarly journals Specific asparagine-linked oligosaccharides are not required for certain neuron-neuron and neuron-Schwann cell interactions.

1986 ◽  
Vol 103 (1) ◽  
pp. 159-170 ◽  
Author(s):  
N Ratner ◽  
A Elbein ◽  
M B Bunge ◽  
S Porter ◽  
R P Bunge ◽  
...  
Keyword(s):  
Schwann Cell ◽  
Schwann Cells ◽  
Normal Structure ◽  
Cell Interactions ◽  
Dorsal Root Ganglion Neurons ◽  
Neuronal Cultures ◽  
Cellular Functions ◽  
Matrix Deposition ◽  
Neuronal Proteins ◽  
Ganglion Neurons

To determine whether specific asparagine-linked (N-linked) oligosaccharides present in cell surface glycoproteins are required for cell-cell interactions within the peripheral nervous system, we have used castanospermine to inhibit maturation of N-linked sugars in cell cultures of neurons or neurons plus Schwann cells. Maximally 10-15% of the N-linked oligosaccharides on neuronal proteins have normal structure when cells are cultured in the presence of 250 micrograms/ml castanospermine; the remaining oligosaccharides are present as immature carbohydrate chains not normally found in these glycoproteins. Although cultures were treated for 2 wk with castanospermine, cells always remained viable and appeared healthy. We have analyzed several biological responses of embryonic dorsal root ganglion neurons, with or without added purified populations of Schwann cells, in the presence of castanospermine. We have observed that a normal complement of mature, N-linked sugars are not required for neurite outgrowth, neuron-Schwann cell adhesion, neuron-induced Schwann cell proliferation, or ensheathment of neurites by Schwann cells. Treatment of neuronal cultures with castanospermine increases the propensity of neurites to fasciculate. Extracellular matrix deposition by Schwann cells and myelination of neurons by Schwann cells are greatly diminished in the presence of castanospermine as assayed by electron microscopy and immunocytochemistry, suggesting that specific N-linked oligosaccharides are required for the expression of these cellular functions.

Human Neurofibromas in Co-Culture with Mouse Neurons

1982 ◽  
Vol 40 ◽  
pp. 194-195
Author(s):  
R.L. Martuza ◽  
T. Liszczak ◽  
A. Okun ◽  
T-Y Wang
Keyword(s):  
Schwann Cell ◽  
Schwann Cells ◽  
Genetic Disorder ◽  
Cranial Nerves ◽  
Sympathetic Nerves ◽  
Acoustic Neuromas ◽  
Spinal Roots ◽  
Neural Crest Origin ◽  
Multiple Abnormalities ◽  
Other Neoplasms

Neurofibromatosis (NF) is an autosomal dominant genetic disorder with a prevalence of 1/3,000 births. The NF mutation causes multiple abnormalities of various cells of neural crest origin. Schwann cell tumors (neurofibromas, acoustic neuromas) are the most common feature of neurofibromatosis although meningiomas, gliomas, and other neoplasms may be seen. The schwann cell tumors commonly develop from the schwann cells associated with sensory or sympathetic nerves or their ganglia. Schwann cell tumors on ventral spinal roots or motor cranial nerves are much less common. Since the sensory neuron membrane is known to contain a mitogenic factor for schwann cells, we have postulated that neurofibromatosis may be due to an abnormal interaction between the nerve and the schwann cell and that this interaction may be hormonally modulated. To test this possibility a system has been developed in which an enriched schwannoma cell culture can be obtained and co-cultured with pure neurons.

scholarly journals Aldose Reductase and the Polyol Pathway in Schwann Cells: Old and New Problems

2021 ◽  
Vol 22 (3) ◽  
pp. 1031
Author(s):  
Naoko Niimi ◽  
Hideji Yako ◽  
Shizuka Takaku ◽  
Sookja K. Chung ◽  
Kazunori Sango
Keyword(s):  
Schwann Cells ◽  
Aldose Reductase ◽  
Critical Role ◽  
Polyol Pathway ◽  
Glucose Flux ◽  
Rate Limiting ◽  
Deficient Mice ◽  
Excess Glucose ◽  
Shed Light ◽  
Immortalized Schwann Cells

Aldose reductase (AR) is a member of the reduced nicotinamide adenosine dinucleotide phosphate (NADPH)-dependent aldo-keto reductase superfamily. It is also the rate-limiting enzyme of the polyol pathway, catalyzing the conversion of glucose to sorbitol, which is subsequently converted to fructose by sorbitol dehydrogenase. AR is highly expressed by Schwann cells in the peripheral nervous system (PNS). The excess glucose flux through AR of the polyol pathway under hyperglycemic conditions has been suggested to play a critical role in the development and progression of diabetic peripheral neuropathy (DPN). Despite the intensive basic and clinical studies over the past four decades, the significance of AR over-activation as the pathogenic mechanism of DPN remains to be elucidated. Moreover, the expected efficacy of some AR inhibitors in patients with DPN has been unsatisfactory, which prompted us to further investigate and review the understanding of the physiological and pathological roles of AR in the PNS. Particularly, the investigation of AR and the polyol pathway using immortalized Schwann cells established from normal and AR-deficient mice could shed light on the causal relationship between the metabolic abnormalities of Schwann cells and discordance of axon-Schwann cell interplay in DPN, and led to the development of better therapeutic strategies against DPN.

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