Autophagy Is Involved in the Reduction of Myelinating Schwann Cell Cytoplasm during Myelin Maturation of the Peripheral Nerve
Open accessAbstract
Peripheral nerve myelination involves dynamic changes in Schwann cell morphology and membrane structure. Recent studies have demonstrated that autophagy regulates organelle biogenesis and plasma membrane dynamics. In the present study, we investigated the role of autophagy in the development and differentiation of myelinating Schwann cells during sciatic nerve myelination. Electron microscopy and biochemical assays have shown that Schwann cells remove excess cytoplasmic organelles during myelination through macroautophagy. Inhibition of autophagy via Schwann cell-specific removal of ATG7, an essential molecule for macroautophagy, using a conditional knockout strategy, resulted in abnormally enlarged abaxonal cytoplasm in myelinating Schwann cells that contained a large number of ribosomes and an atypically expanded endoplasmic reticulum. Small fiber hypermyelination and minor anomalous peripheral nerve functions are observed in this mutant. Rapamycin-induced suppression of mTOR activity during the early postnatal period enhanced not only autophagy but also developmental reduction of myelinating Schwann cells cytoplasm in vivo. Together, our findings suggest that autophagy is a regulatory mechanism of Schwann cells structural plasticity during myelination.
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During development, autophagy is required for refining and culling of Schwann cell-mediated myelination.
“During development, autophagy is required for refining and culling of Schwann cell-mediated myelination,”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [459]
Conditional Atg7 deletion in mouse Schwann cells leads to cytoplasmic swelling, ribosomal accumulation, dysmorphic ER, and dysmyelination.
“and conditional Atg7 deletion in mouse Schwann cells leads to cytoplasmic swelling, ribosomal accumulation, dysmorphic ER, and dysmyelination [459].”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [459]
Myelinophagy is impaired by Schwann cell-specific Atg7 deletion.
“and this function is impaired by Schwann cell-specific Atg7 deletion [459,464].”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [459]
After nerve injury, Schwann cells oversee the capture of myelin debris in autophagosomes in a process termed myelinophagy.
“After nerve injury, Schwann cells oversee the capture of myelin debris in autophagosomes in a process termed “myelinophagy” [459,462,463],”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [459]
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Autophagy in Schwann cells: A potential pharmacotherapeutic target in diabetic peripheral neuropathy
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Neurodegenerative Diseases and Autophagy
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Autophagy and Neurodegenerative Diseases
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Schwann Cell‐Specific ATG7 ‐Dependent Autophagy Protects Myelin in a Mouse Model of Krabbe Disease
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“SCs use autophagy machinery to degrade/clear myelin debris (Gomez-Sanchez et al. 2015; Jang et al. 2015), and autophagy was found to be upregulated in sciatic nerves during mouse development (Jang et al. 2015) when SCs are actively myelinating the axon fibers, suggesting that autophagy might play…”
- Authors
- Jang, S. Y., Shin, Y. K., Park, S. Y., Park, J. Y., Rha, S.-H., Kim, J. K., Lee, H. J., & Park, H. T.
- Affiliations
- Dong-A University (KR)
- Corresponding author
- Park, Hwan Tae
- ORCID
- Venue
- PLOS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2015-01-12
- Volume
- 10
- Issue
- 1
- Pages
- e0116624
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC4291222
- OpenAlex
- W2094606934
- Cited by
- 61
- References
- 23
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 5 · 2023: 6 · 2022: 5 · 2021: 8 · 2020: 4 · 2019: 8 · 2018: 6 · 2017: 6 · 2016: 1 · 2015: 3
- FWCI
- 4.18
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- PLoS ONE (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Research Foundation
- Ministry of Science, ICT and Future Planning
- National Research Foundation of Korea (2014R1A2A2A01002566)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Hereditary Neurological Disorders
- Keywords
- autophagy, myelinating Schwann cells, peripheral nerve myelination, macroautophagy, ATG7, sciatic nerve, endoplasmic reticulum, mTOR, ribosome
- MeSH terms
- Autophagy-Related Protein 7, Animals, Autophagy, Cell Differentiation, Cell Membrane, Cytoplasm, Endoplasmic Reticulum, Microtubule-Associated Proteins, Myelin Sheath, Peripheral Nerves, Ribosomes, Schwann Cells, Mice
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