Schwann cell dedifferentiation-associated demyelination leads to exocytotic myelin clearance in inflammatory segmental demyelination

Glia ◽  
2017 ◽  
Vol 65 (11) ◽  
pp. 1848-1862 ◽  
Author(s):  
So Young Jang ◽  
Byeol-A Yoon ◽  
Yoon Kyung Shin ◽  
Seoug Hoon Yun ◽  
Young Rae Jo ◽  
...  
2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Hwan Tae Park ◽  
Hyun Kyoung Lee ◽  
Yoon Kyung Shin ◽  
Junyang Jung ◽  
Duk Joon Suh ◽  
...  

Glia ◽  
2017 ◽  
Vol 65 (6) ◽  
pp. 864-882 ◽  
Author(s):  
Jennifer Soto ◽  
Paula V. Monje

2018 ◽  
Vol 662 ◽  
pp. 136-141 ◽  
Author(s):  
Fabian Szepanowski ◽  
Leon-Phillip Szepanowski ◽  
Anne K. Mausberg ◽  
Christoph Kleinschnitz ◽  
Bernd C. Kieseier ◽  
...  

2021 ◽  
Vol 14 ◽  
Author(s):  
Bo Jia ◽  
Wei Huang ◽  
Yu Wang ◽  
Peng Zhang ◽  
Zhiwei Wang ◽  
...  

While Nogo protein demonstrably inhibits nerve regeneration in the central nervous system (CNS), its effect on Schwann cells in peripheral nerve repair and regeneration following sciatic nerve injury remains unknown. In this research, We assessed the post-injury expression of Nogo-C in an experimental mouse model of sciatic nerve-crush injury. Nogo-C knockout (Nogo-C–/–) mouse was generated to observe the effect of Nogo-C on sciatic nerve regeneration, Schwann cell apoptosis, and myelin disintegration after nerve injury, and the effects of Nogo-C on apoptosis and dedifferentiation of Schwann cells were observed in vitro. We found that the expression of Nogo-C protein at the distal end of the injured sciatic nerve increased in wild type (WT) mice. Compared with the injured WT mice, the proportion of neuronal apoptosis was significantly diminished and the myelin clearance rate was significantly elevated in injured Nogo-C–/– mice; the number of nerve fibers regenerated and the degree of myelination were significantly elevated in Nogo-C–/– mice on Day 14 after injury. In addition, the recovery of motor function was significantly accelerated in the injured Nogo-C–/– mice. The overexpression of Nogo-C in primary Schwann cells using adenovirus-mediated gene transfer promoted Schwann cells apoptosis. Nogo-C significantly reduced the ratio of c-Jun/krox-20 expression, indicating its inhibition of Schwann cell dedifferentiation. Above all, we hold the view that the expression of Nogo-C increases following peripheral nerve injury to promote Schwann cell apoptosis and inhibit Schwann cell dedifferentiation, thereby inhibiting peripheral nerve regeneration.


2018 ◽  
Vol 38 (29) ◽  
pp. 6546-6562 ◽  
Author(s):  
Yo Sasaki ◽  
Amber R. Hackett ◽  
Sungsu Kim ◽  
Amy Strickland ◽  
Jeffrey Milbrandt

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1366 ◽  
Author(s):  
Benedetta E. Fornasari ◽  
Marwa El Soury ◽  
Giulia Nato ◽  
Alessia Fucini ◽  
Giacomo Carta ◽  
...  

Conduits for the repair of peripheral nerve gaps are a good alternative to autografts as they provide a protected environment and a physical guide for axonal re-growth. Conduits require colonization by cells involved in nerve regeneration (Schwann cells, fibroblasts, endothelial cells, macrophages) while in the autograft many cells are resident and just need to be activated. Since it is known that soluble Neuregulin1 (sNRG1) is released after injury and plays an important role activating Schwann cell dedifferentiation, its expression level was investigated in early regeneration steps (7, 14, 28 days) inside a 10 mm chitosan conduit used to repair median nerve gaps in Wistar rats. In vivo data show that sNRG1, mainly the isoform α, is highly expressed in the conduit, together with a fibroblast marker, while Schwann cell markers, including NRG1 receptors, were not. Primary culture analysis shows that nerve fibroblasts, unlike Schwann cells, express high NRG1α levels, while both express NRG1β. These data suggest that sNRG1 might be mainly expressed by fibroblasts colonizing nerve conduit before Schwann cells. Immunohistochemistry analysis confirmed NRG1 and fibroblast marker co-localization. These results suggest that fibroblasts, releasing sNRG1, might promote Schwann cell dedifferentiation to a “repair” phenotype, contributing to peripheral nerve regeneration.


Author(s):  
Roy O. Weller

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.


2018 ◽  
Vol 38 (20) ◽  
pp. 4811-4828 ◽  
Author(s):  
Camilla Norrmén ◽  
Gianluca Figlia ◽  
Patrick Pfistner ◽  
Jorge A. Pereira ◽  
Sven Bachofner ◽  
...  

Glia ◽  
2015 ◽  
Vol 63 (6) ◽  
pp. 977-986 ◽  
Author(s):  
Janos Groh ◽  
Ines Klein ◽  
Claudia Hollmann ◽  
Jennifer Wettmarshausen ◽  
Dennis Klein ◽  
...  

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