Schwann cells selectively myelinate primary motor axons via neuregulin‐ErbB signaling

Glia ◽  
2020 ◽  
Vol 68 (12) ◽  
pp. 2585-2600
Author(s):  
Dong‐Won Lee ◽  
Eunmi Kim ◽  
Inyoung Jeong ◽  
Hwan‐Ki Kim ◽  
Suhyun Kim ◽  
...  
Keyword(s):  
Schwann Cells ◽  
Motor Axons ◽  
Erbb Signaling

Chemical communication between regenerating motor axons and Schwann cells in the growth pathway

2009 ◽  
Vol 30 (3) ◽  
pp. 366-375 ◽  
Author(s):  
Gerta Vrbova ◽  
Neeraj Mehra ◽  
Harei Shanmuganathan ◽  
Neil Tyreman ◽  
Melitta Schachner ◽  
...  
Keyword(s):  
Schwann Cells ◽  
Chemical Communication ◽  
Motor Axons ◽  
Growth Pathway

scholarly journals Schwann Cells and Deleted in Colorectal Carcinoma Direct Regenerating Motor Axons Towards Their Original Path

2014 ◽  
Vol 34 (44) ◽  
pp. 14668-14681 ◽  
Author(s):  
A. F. Rosenberg ◽  
J. Isaacman-Beck ◽  
C. Franzini-Armstrong ◽  
M. Granato
Keyword(s):  
Colorectal Carcinoma ◽  
Schwann Cells ◽  
Motor Axons ◽  
Deleted In Colorectal Carcinoma

scholarly journals Novel EGR2 variant that associates with Charcot-Marie-Tooth disease when combined with lipopolysaccharide-induced TNF-α factor T49M polymorphism

2020 ◽  
Vol 6 (2) ◽  
pp. e407
Author(s):  
Maria Empar Blanco-Cantó ◽  
Nikiben Patel ◽  
Sergio Velasco-Aviles ◽  
Angeles Casillas-Bajo ◽  
Juan Salas-Felipe ◽  
...  
Keyword(s):  
Peripheral Neuropathy ◽  
Schwann Cells ◽  
Loss Of Function ◽  
Charcot Marie Tooth ◽  
Charcot Marie Tooth Disease ◽  
Tnf Α ◽  
Erbb Signaling ◽  
Steady State Levels ◽  
Schwann Cell Differentiation

ObjectiveTo identify novel genetic mechanisms causing Charcot-Marie-Tooth (CMT) disease.MethodsWe performed a next-generation sequencing study of 34 genes associated with CMT in a patient with peripheral neuropathy.ResultsWe found a non–previously described mutation in EGR2 (p.P397H). P397H mutation is located within the loop that connects zinc fingers 2 and 3, a pivotal domain for the activity of this transcription factor. Using promoter activity luciferase assays, we found that this mutation promotes decreased transcriptional activity of EGR2. In this patient, we also found a previously described nonpathogenic polymorphism in lipopolysaccharide-induced TNF-α factor (LITAF) (p.T49M). We show that the p.T49M mutation decreases the steady-state levels of the LITAF protein in Schwann cells. Loss of function of LITAF has been shown to produce deregulation in the NRG1-erbB signaling, a pivotal pathway for EGR2 expression by Schwann cells. Surprisingly, our segregation study demonstrates that p.P397H mutation in EGR2 is not sufficient to produce CMT disease. Most notably, only those patients expressing simultaneously the LITAF T49M polymorphism develop peripheral neuropathy.ConclusionsOur data support that the LITAF loss-of-function interferes with the expression of the transcriptional-deficient EGR2 P397H mutant hampering Schwann cell differentiation and suggest that in vivo both genes act in tandem to allow the proper development of myelin.

Axons arrest the migration of Schwann cell precursors

Development ◽  
1994 ◽  
Vol 120 (6) ◽  
pp. 1411-1420 ◽  
Author(s):  
A. Bhattacharyya ◽  
R. Brackenbury ◽  
N. Ratner
Keyword(s):  
Schwann Cell ◽  
Motor Neuron ◽  
Neural Crest ◽  
Schwann Cells ◽  
Neural Tube ◽  
Neural Crest Cells ◽  
Ventral Root ◽  
Motor Axons ◽  
Ventral Neural Tube ◽  
Schwann Cell Precursors

The neural crest gives rise to a variety of cell types including Schwann cells of the peripheral nervous system. Schwann cell precursors begin to differentiate early and migrate along specific pathways in the embryo before associating with nerve trunks. To determine whether motor axons direct the migration of Schwann cell precursors along specific pathways, we tested the effect of ablating the ventral half of the neural tube, which contains motor neuron cell bodies. The ventral neural tube was removed unilaterally from lumbar regions of chicken embryos at stage 17, when neural crest cells are just beginning to migrate and before motor axons have extended out of the neural tube. At several stages after ventral tube ablation, sections of the lumbar region of these embryos were stained with anti-acetylated tubulin to label developing axons, HNK-1 to label migrating neural crest cells and 1E8 to label Schwann cell precursors. In many embryos the ablation of motor neurons was incomplete. The staining patterns in these embryos support the idea that some Schwann cells are derived from the neural tube. In embryos with complete motor neuron ablation, at stage 18, HNK-1-positive neural crest cells had migrated to normal locations in both control and ablated sides of the embryo, suggesting that motor axons or the ventral neural tube are not required for proper migration of neural crest cells. However, by stage 19, cells that were positive for HNK-1 or 1E8 were no longer seen in the region of the ventral root, nor ventral to the ventral root region. Because Schwann cell precursors require neural-derived factors for their survival in vitro, we tested whether neural crest cells that migrate to the region of the ventral root in ventral neural tube-ablated embryos then die. Nile Blue staining for dead and dying cells in ventral neural tube-ablated embryos provided no evidence for cell death at stage 18. These results suggest that motor axons arrest the migration of Schwann cell precursors during neural crest migration.

Ultrastructure of Giant Mitochondria and Their Inclusions in Schwann Cells of Bovine Splenic Nerve

1974 ◽  
Vol 32 ◽  
pp. 194-195
Author(s):  
Å. Thureson-Klein
Keyword(s):  
Schwann Cells ◽  
Cell Organelles ◽  
Giant Mitochondria ◽  
Matrix Density ◽  
Physiological Conditions ◽  
Unmyelinated Axons ◽  
Internal Structures ◽  
Structural Abnormalities ◽  
Cytotoxic Compounds ◽  
Cell Components

Giant mitochondria of various shapes and with different internal structures and matrix density have been observed in a great number of tissues including nerves. In most instances, the presence of giant mitochondria has been associated with a known disease or with abnormal physiological conditions such as anoxia or exposure to cytotoxic compounds. In these cases degenerative changes occurred in other cell organelles and, therefore the giant mitochondria also were believed to be induced structural abnormalities.Schwann cells ensheating unmyelinated axons of bovine splenic nerve regularly contain giant mitochondria in addition to the conventional smaller type (Fig. 1). These nerves come from healthy inspected animals presumed not to have been exposed to noxious agents. As there are no drastic changes in the small mitochondria and because other cell components also appear reasonably well preserved, it is believed that the giant mitochondria are normally present jin vivo and have not formed as a post-mortem artifact.

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.

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