The response of the (myelinating) Schwann cell population to multiple episodes of demyelination

1983 ◽  
Vol 12 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Susan M. Hall
Keyword(s):  
Schwann Cell ◽  
Cell Population ◽  
Myelinating Schwann Cell ◽  
Multiple Episodes

Characterisation of cis-acting sequences reveals a biphasic, axon-dependent regulation of Krox20 during Schwann cell development

Development ◽  
2002 ◽  
Vol 129 (1) ◽  
pp. 155-166 ◽  
Author(s):  
Julien Ghislain ◽  
Carole Desmarquet-Trin-Dinh ◽  
Martine Jaegle ◽  
Dies Meijer ◽  
Patrick Charnay ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Schwann Cell ◽  
Dependent Manner ◽  
Cis Acting ◽  
Pou Domain ◽  
Cell Element ◽  
Schwann Cell Development ◽  
Myelinating Schwann Cell ◽  
Sciatic Nerve Regeneration

In Schwann cells (SC), myelination is controlled by the transcription factor gene Krox20/Egr2. Analysis of cis-acting elements governing Krox20 expression in SC revealed the existence of two separate elements. The first, designated immature Schwann cell element (ISE), was active in immature but not myelinating SC, whereas the second, designated myelinating Schwann cell element (MSE), was active from the onset of myelination to adulthood in myelinating SC. In vivo sciatic nerve regeneration experiments demonstrated that both elements were activated during this process, in an axon-dependent manner. Together the activity of these elements reproduced the profile of Krox20 expression during development and regeneration. Genetic studies showed that both elements were active in a Krox20 mutant background, while the activity of the MSE, but likely not of the ISE, required the POU domain transcription factor Oct6 at the time of myelination. The MSE was localised to a 1.3 kb fragment, 35 kb downstream of Krox20. The identification of multiple Oct6 binding sites within this fragment suggested that Oct6 directly controls Krox20 transcription. Taken together, these data indicate that, although Krox20 is expressed continuously from 15.5 dpc in SC, the regulation of its expression is a biphasic, axon-dependent phenomenon involving two cis-acting elements that act in succession during development. In addition, they provide insight into the complexity of the transcription factor regulatory network controlling myelination.

scholarly journals Polarization of myelinating Schwann cell surface membranes: role of microtubules and the trans-Golgi network

1995 ◽  
Vol 15 (3) ◽  
pp. 1797-1807 ◽  
Author(s):  
BD Trapp ◽  
GJ Kidd ◽  
P Hauer ◽  
E Mulrenin ◽  
CA Haney ◽  
...  
Keyword(s):  
Schwann Cell ◽  
Cell Surface ◽  
Trans Golgi Network ◽  
Myelinating Schwann Cell ◽  
Golgi Network

scholarly journals Myelin-associated glycoprotein and myelinating Schwann cell-axon interaction in chronic B,B'-iminodipropionitrile neuropathy.

1984 ◽  
Vol 98 (4) ◽  
pp. 1272-1278 ◽  
Author(s):  
B D Trapp ◽  
R H Quarles ◽  
J W Griffin
Keyword(s):  
Schwann Cell ◽  
Central Zone ◽  
Minor Component ◽  
Outer Zone ◽  
Structural Protein ◽  
Myelinated Fibers ◽  
Pns Myelin ◽  
Myelin Associated Glycoprotein ◽  
Myelinating Schwann Cell ◽  
Periaxonal Space

The myelin-associated glycoprotein (MAG) is a heavily glycosylated integral membrane glycoprotein which is a minor component of isolated rat peripheral nervous system (PNS) myelin. Immunocytochemically MAG has been localized in the periaxonal region of PNS myelin sheaths. The periaxonal localization and biochemical features of MAG are consistent with the hypothesis that MAG plays a role in maintaining the periaxonal space of myelinated fibers. To test this hypothesis, MAG was localized immunocytochemically in 1-micron sections of the L5 ventral root from rats exposed to B,B'-iminodipropionitrile. In chronic states of B,B'-iminodipropionitrile intoxication, Schwann cell periaxonal membranes and the axolemma invaginate into giant axonal swellings and separate a central zone of normally oriented axoplasm from an outer zone of maloriented neurofilaments. Ultrastructurally, the width of the periaxonal space (12-14 nm) in the ingrowths is identical to that found in normally myelinated fibers. These Schwann cell ingrowths which are separated from compact myelin by several micra are stained intensely by MAG antiserum. Antiserum directed against Po protein, the major structural protein of compact PNS myelin, does not stain the ingrowths unless compact myelin is present. These results demonstrate the periaxonal localization of MAG and support a functional role for MAG in maintaining the periaxonal space of PNS myelinated fibers.

scholarly journals HDAC3 Regulates the Transition to the Homeostatic Myelinating Schwann Cell State

Cell Reports ◽  
2018 ◽  
Vol 25 (10) ◽  
pp. 2755-2765.e5 ◽  
Author(s):  
Laura H. Rosenberg ◽  
Anne-Laure Cattin ◽  
Xavier Fontana ◽  
Elizabeth Harford-Wright ◽  
Jemima J. Burden ◽  
...  
Keyword(s):  
Schwann Cell ◽  
Cell State ◽  
Myelinating Schwann Cell

scholarly journals Normal basal laminas are realized on dystrophic Schwann cells in dystrophic in equilibrium shiverer chimera nerves.

1984 ◽  
Vol 99 (5) ◽  
pp. 1831-1837 ◽  
Author(s):  
A C Peterson ◽  
G M Bray
Keyword(s):  
Schwann Cell ◽  
Schwann Cells ◽  
Cell Population ◽  
Basal Lamina ◽  
Mutant Phenotype ◽  
Normal Product ◽  
Pathogenetic Mechanisms ◽  
Dystrophic Mice

Multiple discontinuities are observed in the basal laminas of Schwann cells in mature dystrophic mice. To explore the pathogenesis of this abnormality we have exploited a dystrophic in equilibrium shiverer mouse chimera preparation in which both the basal lamina phenotype and the genotype of myelin-forming Schwann cells can be determined. If the basal lamina abnormality were to arise from an intrinsic deficiency of the dystrophic Schwann cell itself, only those Schwann cells of dystrophic genotype could express the mutant phenotype, whereas the coexisting population of shiverer Schwann cells should express typically normal basal laminas. No such distinction was observed; rather both dystrophic and shiverer Schwann cells were found to express relatively normal basal laminas and two pathogenetic mechanisms remain theoretical possibilities. The dystrophic Schwann cell population may be intrinsically defective but also may be rescued by obtaining the normal product of the dy locus synthesized by the coexisting shiverer cells. Alternatively, an extra Schwann cell deficiency existing within dystrophic mice may be normalized by shiverer cells and the normal intrinsic potential of both dystrophic and shiverer Schwann cells can then be realized. Regardless of the exact mechanism underlying these findings, some extracellularly mediated influence, emanating in vivo from shiverer cells, is capable of ameliorating the basal lamina deficiency typically expressed by dystrophic Schwann cells.

scholarly journals c-Jun is a negative regulator of myelination

2008 ◽  
Vol 181 (4) ◽  
pp. 625-637 ◽  
Author(s):  
David B. Parkinson ◽  
Ambily Bhaskaran ◽  
Peter Arthur-Farraj ◽  
Luke A. Noon ◽  
Ashwin Woodhoo ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Schwann Cell ◽  
Cell Biology ◽  
Gene Activation ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Negative Regulator ◽  
Cell Phenotype ◽  
Myelinating Schwann Cell

Schwann cell myelination depends on Krox-20/Egr2 and other promyelin transcription factors that are activated by axonal signals and control the generation of myelin-forming cells. Myelin-forming cells remain remarkably plastic and can revert to the immature phenotype, a process which is seen in injured nerves and demyelinating neuropathies. We report that c-Jun is an important regulator of this plasticity. At physiological levels, c-Jun inhibits myelin gene activation by Krox-20 or cyclic adenosine monophosphate. c-Jun also drives myelinating cells back to the immature state in transected nerves in vivo. Enforced c-Jun expression inhibits myelination in cocultures. Furthermore, c-Jun and Krox-20 show a cross-antagonistic functional relationship. c-Jun therefore negatively regulates the myelinating Schwann cell phenotype, representing a signal that functionally stands in opposition to the promyelin transcription factors. Negative regulation of myelination is likely to have significant implications for three areas of Schwann cell biology: the molecular analysis of plasticity, demyelinating pathologies, and the response of peripheral nerves to injury.

scholarly journals Distribution and role in regeneration of N-CAM in the basal laminae of muscle and Schwann cells.

1988 ◽  
Vol 107 (2) ◽  
pp. 707-719 ◽  
Author(s):  
F Rieger ◽  
M Nicolet ◽  
M Pinçon-Raymond ◽  
M Murawsky ◽  
G Levi ◽  
...  
Keyword(s):  
Schwann Cell ◽  
Nerve Regeneration ◽  
Schwann Cells ◽  
Basal Lamina ◽  
Close Association ◽  
Axon Terminals ◽  
Muscle Extract ◽  
Cell Processes ◽  
Myelinating Schwann Cell

The neural cell adhesion molecule (N-CAM) is a membrane glycoprotein involved in neuron-neuron and neuron-muscle adhesion. It can be synthesized in various forms by both nerve and muscle and it becomes concentrated at the motor endplate. Biochemical analysis of a frog muscle extract enriched in basal lamina revealed the presence of a polydisperse, polysialylated form of N-CAM with an average Mr of approximately 160,000 as determined by SDS-PAGE, which was converted to a form of 125,000 Mr by treatment with neuraminidase. To define further the role of N-CAM in neuromuscular junction organization, we studied the distribution of N-CAM in an in vivo preparation of frog basal lamina sheaths obtained by inducing the degeneration of both nerve and muscle fibers. Immunoreactive material could be readily detected by anti-N-CAM antibodies in such basal lamina sheaths. Ultrastructural analysis using immunogold techniques revealed N-CAM in close association with the basal lamina sheaths, present in dense accumulation at places that presumably correspond to synaptic regions. N-CAM epitopes were also associated with collagen fibrils in the extracellular matrix. The ability of anti-N-CAM antibodies to perturb nerve regeneration and reinnervation of the remaining basal lamina sheaths was then examined. In control animals, myelinating Schwann cells wrapped around the regenerated axon and reinnervation occurred only at the old synaptic areas; new contacts between nerve and basal lamina had a terminal Schwann cell capping the nerve terminal. In the presence of anti-N-CAM antibodies, three major abnormalities were observed in the regeneration and reinnervation processes: (a) regenerated axons in nerve trunks that had grown back into the old Schwann cell basal lamina were rarely associated with myelinating Schwann cell processes, (b) ectopic synapses were often present, and (c) many of the axon terminals lacked a terminal Schwann cell capping the nerve-basal lamina contact area. These results suggest that N-CAM may play an important role not only in the determination of synaptic areas but also in Schwann cell-axon interactions during nerve regeneration.

Guiding Mesenchymal Stem Cells into Myelinating Schwann Cell-Like Phenotypes by Using Electrospun Core–Sheath Nanoyarns

2019 ◽  
Vol 5 (10) ◽  
pp. 5284-5294 ◽  
Author(s):  
Shaohua Wu ◽  
Shilei Ni ◽  
Xiping Jiang ◽  
Mitchell A. Kuss ◽  
Han-Jun Wang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Schwann Cell ◽  
Myelinating Schwann Cell
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