c-Jun expression in human neuropathies: a pilot study
Abstract
Schwann cell dedifferentiation following nerve injury is important to permit neural survival and axonal regrowth. Animal studies have shown that the transcription factor c-Jun is upregulated in Schwann cells of injured and pathological nerves where it acts as an important regulator of Schwann cell plasticity, promoting dedifferentiation and demyelination. This pilot immunohistochemical study investigates whether c-Jun is also upregulated in human neuropathies. We examined c-Jun expression in normal and diseased human nerves, as well as in dermal myelinated nerve fibres. Our findings show that although as predicted c-Jun is rarely expressed in normal nerves, it is expressed in Schwann cell nuclei of pathological nerves as predicted by animal studies. Pathological dermal myelinated nerve fibres also show clear nuclear c-Jun expression. Further studies of c-Jun expression will help clarify its role in human neuropathies.
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Higher JUN/c-Jun in CMT1A may be part of a compensatory, neuroprotective response to the pathogenic effects of the PMP22 duplication.
“which may be part of a compensatory, neuroprotective response to the pathogenic effects of the PMP22 duplication [467–469].”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [468]
In Charcot-Marie-Tooth type 1A caused by duplication of PMP22, Schwann cell autophagy is aberrantly elevated.
“in Charcot-Marie-Tooth (CMT) type 1A caused by duplication of PMP22 (peripheral myelin protein 22), Schwann cell autophagy is aberrantly elevated”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [468]
In CMT1A, elevated Schwann cell autophagy is associated with higher levels of JUN/c-Jun.
“and associated with higher levels of JUN/c-Jun,”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [468]
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- Authors
- Hutton, E. J., Carty, L., Laurá, M., Houlden, H., Lunn, M. P. T., Brandner, S., Mirsky, R., Jessen, K., & Reilly, M. M.
- Affiliations
- UCL Queen Square Institute of Neurology (GB)
- Corresponding author
- Hutton, Elspeth J.
- ORCID
- Venue
- Journal of the Peripheral Nervous System
- Publisher
- Wiley
- Published
- 2011-12
- Volume
- 16
- Issue
- 4
- Pages
- 295-303
- ISSN
- 1085-9489 (ISSN-L)
- OpenAlex
- W2131191664
- Cited by
- 63
- References
- 19
- Citations by year
- 2025: 1 · 2024: 3 · 2023: 7 · 2022: 2 · 2021: 5 · 2020: 3 · 2019: 7 · 2018: 4 · 2017: 9 · 2016: 3 · 2015: 4 · 2014: 5 · 2013: 3 · 2012: 7
- FWCI
- 1.99
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of the Peripheral Nervous System (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (U54NS065712)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Health Sciences › Medicine › Neurology › Peripheral Neuropathies and Disorders
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Hereditary Neurological Disorders
- Keywords
- c-Jun, Schwann cells, Schwann cell dedifferentiation, neuropathy, demyelination, myelinated axons, nerve injury, transcription factor expression, peripheral nerve pathology
- MeSH terms
- Adult, Aged, Aged, 80 and over, Female, Humans, Immunohistochemistry, Infant, Male, Middle Aged, Nerve Fibers, Myelinated, Peripheral Nervous System Diseases, Pilot Projects, Schwann Cells, Skin, Proto-Oncogene Proteins c-jun, Young Adult
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