Schwann cell dedifferentiation-associated demyelination leads to exocytotic myelin clearance in inflammatory segmental demyelination
Abstract
Schwann cells (SCs), which form the peripheral myelin sheath, have the unique ability to dedifferentiate and to destroy the myelin sheath under various demyelination conditions. During SC dedifferentiation-associated demyelination (SAD) in Wallerian degeneration (WD) after axonal injury, SCs exhibit myelin and junctional instability, down-regulation of myelin gene expression and autophagic myelin breakdown. However, in inflammatory demyelinating neuropathy (IDN), it is still unclear how SCs react and contribute to segmental demyelination before myelin scavengers, macrophages, are activated for phagocytotic myelin digestion. Here, we compared the initial SC demyelination mechanism of IDN to that of WD using microarray and histochemical analyses and found that SCs in IDN exhibited several typical characteristics of SAD, including actin-associated E-cadherin destruction, without obvious axonal degeneration. However, autophagolysosome activation in SAD did not appear to be involved in direct myelin lipid digestion by SCs but was required for the separation of SC body from destabilized myelin sheath in IDN. Thus, lysosome inhibition in SCs suppressed segmental demyelination by preventing the exocytotic myelin clearance of SCs. In addition, we found that myelin rejection, which might also require the separation of SC cytoplasm from destabilized myelin sheath, was delayed in SC-specific Atg7 knockout mice in WD, suggesting that autophagolysosome-dependent exocytotic myelin clearance by SCs in IDN and WD is a shared mechanism. Finally, autophagolysosome activation in SAD was mechanistically dissociated with the junctional destruction in both IDN and WD. Thus, our findings indicate that SAD could be a common myelin clearance mechanism of SCs in various demyelinating conditions.
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Myelinophagy is impaired by Schwann cell-specific Atg7 deletion.
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Wu, Z., Yan, W., Wang, K., Xu, G., Zhu, D., Li, X., Wang, H., Yang, M., Zhang, X., & Wu, J. (2023) · Archives of Toxicology · doi:10.1007/s00204-023-03468-6 · Cited by 12 · see citing works
Serum CXCL13 reflects local B-cell mediated inflammatory demyelinating peripheral neuropathy
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Lysosomal dysfunction in Schwann cells is involved in bortezomib-induced peripheral neuropathyPreprint
Wu, Z., Yan, W., Wang, K., Xu, G., Zhu, D., Li, X., Wang, H., Yang, M., Zhang, X., & Wu, J. (2022) · Research Square · doi:10.21203/rs.3.rs-2241499/v1
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Mechanisms and therapeutic strategies for central and peripheral remyelination
Zhan, J., Jo, J., Cristobal, C. D., Jeong, D. J., Park, H. T., & Lee, H. K. (2026) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2026.102964
Self-citation
- Authors
- Jang, S. Y., Yoon, B.-A., Shin, Y. K., Yun, S. H., Jo, Y. R., Choi, Y. Y., Ahn, M., Shin, T., Park, J. I., Kim, J. K., & Park, H. T.
- Affiliations
- Dong-A University (KR)
- Jeju National University (KR)
- Corresponding author
- Park, Hwan Tae
- ORCID
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2017-08-10
- Volume
- 65
- Issue
- 11
- Pages
- 1848-1862
- ISSN
- 0894-1491 (ISSN-L)
- OpenAlex
- W2744795364
- Cited by
- 46
- References
- 66
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 4 · 2023: 7 · 2022: 3 · 2021: 6 · 2020: 3 · 2019: 9 · 2018: 5
- FWCI
- 3.24
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Glia (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Research Foundation of Korea (2014R1A2A2A01002566, 2016R1A5A2007009)
- Korean Health Technology R&D Project, Ministry of Health & Welfare (HI14C18070000)
- Topics
- Health Sciences › Medicine › Neurology › Peripheral Neuropathies and Disorders
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- Schwann cell dedifferentiation, segmental demyelination, inflammatory demyelinating neuropathy, Wallerian degeneration, autophagolysosomes, ATG7, E-cadherin
- MeSH terms
- Autophagy-Related Protein 7, Animals, Chloroquine, Demyelinating Diseases, Disease Models, Animal, Female, Male, Mice, Inbred C57BL, Mice, Transgenic, Myelin Proteins, Nerve Tissue Proteins, Neuritis, Autoimmune, Experimental, Rats, Inbred Lew, Schwann Cells, Down-Regulation, Axotomy, Sciatic Neuropathy, Mice, Rats, Cell Dedifferentiation, Receptors, Urokinase Plasminogen Activator
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