{
  "abstract": "Various soluble factors, such as inflammatory cytokines and autoantibodies secreted by activated microglia, macrophages, and astrocytes, are known to promote death of oligodendrocyte (OL) lineage cells, including OLs and OL precursor cells (OPCs), in the central nervous system during demyelination of multiple sclerosis. However, the role of factors secreted by neurons in OL lineage cell death remains underexplored. Chromogranin B (Chgb), a critical protein for secretory granule formation in neuroendocrine cells, is also specifically expressed and secreted from neurons. In this study, we investigated the effect of extracellular Chgb on OL lineage cells. We found that treatment with recombinant mouse or human Chgb significantly reduced the population of both mature OLs and OPCs by inducing apoptosis. This Chgb-induced apoptosis was effectively suppressed by an anti-Chgb antibody. Furthermore, in neuron-OPC/OL cocultures, endogenous Chgb secreted by neurons similarly promoted OL apoptosis, an effect that was also neutralized by the anti-Chgb antibody. Collectively, these results identify Chgb as a neuronal paracrine factor that triggers apoptotic death in OL lineage cells. Our findings provide new insights into the regulation of OL lineage cell death by neuronal secretion factors.",
  "abstract_shown": true,
  "affiliations": [
    "Department of Clinical Bioanalysis and Molecular Biology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo/Tokyo Medical and Dental University (TMDU), Tokyo, Japan",
    "Department of Molecular and Cellular Biology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo/TMDU, Tokyo, Japan"
  ],
  "article_type": "Research Article",
  "arxiv": null,
  "author_total": 9,
  "authors": [
    {
      "affs": [
        0
      ],
      "name": "Nanako Yamada"
    },
    {
      "affs": [
        1
      ],
      "name": "Momona Yamada"
    },
    {
      "name": "Reina Ono"
    },
    {
      "name": "Binri Sasaki"
    },
    {
      "name": "Sakurako Abe"
    },
    {
      "name": "Tomoka Aoki"
    },
    {
      "name": "Akira Yoshimoto"
    },
    {
      "name": "Ryunosuke Ohkawa"
    },
    {
      "name": "Nobuharu Suzuki"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/3mthtjw2jbmtz.bib",
  "cited_by": 0,
  "doi": "10.1371/journal.pone.0358362",
  "fulltext_url": null,
  "id": "3mthtjw2jbmtz",
  "issns": [
    "1932-6203"
  ],
  "landing_url": "https://doi.org/10.1371/journal.pone.0358362",
  "language": null,
  "licence": "CC-BY-4.0",
  "licence_label": "CC BY 4.0",
  "licence_source": "journal",
  "licence_url": "https://creativecommons.org/licenses/by/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "openalex",
      "2734|Multiple Sclerosis Research Studies"
    ],
    [
      "plos",
      "/Biology and life sciences/Cell biology/Cell processes/Cell death/Apoptosis"
    ],
    [
      "plos",
      "/Biology and life sciences/Cell biology/Cell processes/Cell death/Neuronal death"
    ],
    [
      "plos",
      "/Biology and life sciences/Cell biology/Cellular types/Animal cells/Neurons"
    ],
    [
      "plos",
      "/Biology and life sciences/Developmental biology/Cell differentiation"
    ],
    [
      "plos",
      "/Biology and life sciences/Developmental biology/Cell differentiation/Neuronal differentiation"
    ],
    [
      "plos",
      "/Biology and life sciences/Immunology/Clinical immunology/Autoimmune diseases/Multiple sclerosis"
    ],
    [
      "plos",
      "/Biology and life sciences/Neuroscience/Cellular neuroscience/Neurons"
    ],
    [
      "plos",
      "/Medicine and health sciences/Clinical medicine/Clinical immunology/Autoimmune diseases/Multiple sclerosis"
    ],
    [
      "plos",
      "/Medicine and health sciences/Immunology/Clinical immunology/Autoimmune diseases/Multiple sclerosis"
    ],
    [
      "plos",
      "/Medicine and health sciences/Medical conditions/Demyelinating disorders/Multiple sclerosis"
    ],
    [
      "plos",
      "/Medicine and health sciences/Medical conditions/Neurodegenerative diseases/Multiple sclerosis"
    ],
    [
      "plos",
      "/Medicine and health sciences/Neurology/Demyelinating disorders/Multiple sclerosis"
    ],
    [
      "plos",
      "/Medicine and health sciences/Neurology/Neurodegenerative diseases/Multiple sclerosis"
    ],
    [
      "plos",
      "/Research and analysis methods/Specimen preparation and treatment/Staining/Immunostaining"
    ],
    [
      "plos",
      "/Research and analysis methods/Specimen preparation and treatment/Staining/Nuclear staining/DAPI staining"
    ]
  ],
  "openalex": "W7213938298",
  "pdf_url": "https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0358362&type=printable",
  "pmcid": null,
  "pmid": null,
  "published": "2026-09-21",
  "publisher": "Public Library of Science",
  "ris": "https://research.draconitic.com/paper/3mthtjw2jbmtz.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:17:43Z",
      "native_id": "10.1371/journal.pone.0358362",
      "source": "plos",
      "url": "https://doi.org/10.1371/journal.pone.0358362"
    }
  ],
  "subjects": [
    {
      "field": "biology",
      "origin": "plos:cell biology",
      "subfield": "cell-biology"
    },
    {
      "field": "biology",
      "origin": "plos:developmental biology",
      "subfield": "developmental-biology"
    },
    {
      "field": "biology",
      "origin": "plos:immunology",
      "subfield": "immunology"
    }
  ],
  "title": "Chromogranin B acts as a neuronal paracrine factor to trigger oligodendrocyte apoptosis",
  "title_text": "Chromogranin B acts as a neuronal paracrine factor to trigger oligodendrocyte apoptosis",
  "type": "peer-reviewed",
  "updated_at": "2026-10-30T12:17:43Z",
  "url": "https://research.draconitic.com/paper/3mthtjw2jbmtz",
  "venue": "PLOS One",
  "versions": []
}