ArticleBrain pathology (Zurich, Switzerland)2022
Ermin deficiency leads to compromised myelin, inflammatory milieu, and susceptibility to demyelinating insult.
Article in Brain pathology (Zurich, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 20 citations in OpenAlex.
- Dysregulated lipid metabolism and hypomyelination in postnatal peroxisome-deficientFrontiers in molecular neuroscience · 2026Article
- Proteomic Characterization of Spinal Cord Myelin in the Mouse.ASN neuro · 2026Article
- Myelin regulatory factor (MYRF) is a critical early regulator of retinal pigment epithelial development.PLoS genetics · 2025Article
- Akkermansia mono-colonization modulates microglia and astrocytes in a strain specific manner.Journal of neuroinflammation · 2025Article
- Intracellular spatial transcriptomic analysis toolkit (InSTAnT).Nature communications · 2024Article
- Proteomics analysis of periplaque and chronic inactive multiple sclerosis lesions.Frontiers in molecular neuroscience · 2024Article
- Emergence of the brain-border immune niches and their contribution to the development of neurodegenerative diseases.Frontiers in immunology · 2024Review
- The Heterogeneous Multiple Sclerosis Lesion: How Can We Assess and Modify a Degenerating Lesion?International journal of molecular sciences · 2023Review
- Intracellular Spatial Transcriptomic Analysis Toolkit (InSTAnT).Research square · 2023Article
- Ermin deficiency leads to compromised myelin, inflammatory milieu, and susceptibility to demyelinating insult.Brain pathology (Zurich, Switzerland) · 2022Article
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Authors and funding
23 authors at 3 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ermin is an actin-binding protein found almost exclusively in the central nervous system (CNS) as a component of myelin sheaths. Although Ermin has been predicted to play a role in the formation and stability of myelin sheaths, this has not been directly examined in vivo. Here, we show that Ermin is essential for myelin sheath integrity and normal saltatory conduction. Loss of Ermin in mice caused de-compacted and fragmented myelin sheaths and led to slower conduction along with progressive neurological deficits. RNA sequencing of the corpus callosum, the largest white matter structure in the CNS, pointed to inflammatory activation in aged Ermin-deficient mice, which was corroborated by increased levels of microgliosis and astrogliosis. The inflammatory milieu and myelin abnormalities were further associated with increased susceptibility to immune-mediated demyelination insult in Ermin knockout mice. Supporting a possible role of Ermin deficiency in inflammatory white matter disorders, a rare inactivating mutation in the ERMN gene was identified in multiple sclerosis patients. Our findings demonstrate a critical role for Ermin in maintaining myelin integrity. Given its near-exclusive expression in myelinating oligodendrocytes, Ermin deficiency represents a compelling "inside-out" model of inflammatory dysmyelination and may offer a new paradigm for the development of myelin stability-targeted therapies.
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