{"doi":"10.1038/nn738","title":"TNFα promotes proliferation of oligodendrocyte progenitors and remyelination","abstract":null,"journal":"Nature Neuroscience","year":2001,"id":47537,"datarank":12.396305992952785,"base_score":6.906754778648554,"endowment":6.906754778648554,"self_citation_contribution":1.0360132167972833,"citation_network_contribution":11.360292776155502,"self_endowment_contribution":1.0360132167972833,"citer_contribution":11.360292776155502,"corpus_percentile":null,"corpus_rank":null,"citation_count":998,"citer_count":200,"citers_with_citation_signal":200,"citers_with_endowment":200,"datacite_reuse_total":14,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":219934,"name":"Jeff Mason","orcid":null,"position":1,"is_corresponding":false},{"id":219935,"name":"Mike Marino","orcid":null,"position":2,"is_corresponding":false},{"id":219936,"name":"Kinuko Suzuki","orcid":null,"position":3,"is_corresponding":false},{"id":219937,"name":"Glenn K. Matsushima","orcid":null,"position":4,"is_corresponding":false},{"id":219938,"name":"Jenny P.-Y. Ting","orcid":null,"position":5,"is_corresponding":false},{"id":106129,"name":"Heather A. Arnett","orcid":"0000-0002-8442-3312","position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"TNFα promotes proliferation of oligodendrocyte progenitors and remyelination","abstract":"Here we used mice lacking tumor necrosis factor-alpha (TNF alpha) and its associated receptors to study a model of demyelination and remyelination in which these events could be carefully controlled using a toxin, cuprizone. Unexpectedly, the lack of TNF alpha led to a significant delay in remyelination as assessed by histology, immunohistochemistry for myelin proteins and electron microscopy coupled with morphometric analysis. Failure of repair correlated with a reduction in the pool of proliferating oligodendrocyte progenitors (bromodeoxyuridine-labeled NG2(+) cells) followed by a reduction in the number of mature oligodendrocytes. Analysis of mice lacking TNF receptor 1 (TNFR1) or TNFR2 indicated that TNFR2, not TNFR1, is critical to oligodendrocyte regeneration. This unexpected reparative role for TNF alpha in the CNS is important for understanding oligodendrocyte regeneration/proliferation, nerve remyelination and the design of new therapeutics for demyelinating diseases.","is_dataset_classified":null,"base_score":6.906754778648554,"endowment":6.906754778648554,"datacite_reuse_total":14,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"11600888","pmcid":null,"openalex_id":"https://openalex.org/W1509596990","authors":[],"funders":[{"funder_name":"NINDS NIH HHS","grant_id":"NS34190","title":null},{"funder_name":"National Institutes of Health","grant_id":"5R01NS034190-08","title":"Role of Class II MHC Antigens in Neurologic Diseases"},{"funder_name":"National Institutes of Health","grant_id":"5R01NS024453-17","title":"Experimental Pathology of Developing Nervous System"}],"total_grants":3,"fwci":10.0516,"citation_percentile":0.98197038,"influential_citations":17,"citation_trend":[{"year":2012,"count":51},{"year":2013,"count":45},{"year":2014,"count":45},{"year":2015,"count":42},{"year":2016,"count":36},{"year":2017,"count":38},{"year":2018,"count":34},{"year":2019,"count":42},{"year":2020,"count":43},{"year":2021,"count":43},{"year":2022,"count":40},{"year":2023,"count":38},{"year":2024,"count":39},{"year":2025,"count":30},{"year":2026,"count":20}],"oa_status":"closed","license":"Springer TDM","oa_locations":[{"url":"http://www.nature.com/articles/nn738.pdf","host_type":"publisher"},{"url":"http://www.nature.com/articles/nn738","host_type":"publisher"},{"url":"https://doi.org/10.1038/nn738","host_type":"journal"},{"url":"https://pubmed.ncbi.nlm.nih.gov/11600888","host_type":"repository"},{"url":"https://dx.doi.org/10.1038/nn738","host_type":""}],"fields_of_study":["Neurogenesis and neuroplasticity mechanisms","Neuroinflammation and Neurodegeneration Mechanisms","Immune cells in cancer","Biology","Medicine","0301 basic medicine","0303 health sciences","03 medical and health sciences","Animals","Antigens, CD","Apoptosis","B-Lymphocytes","Brain Chemistry","Corpus Callosum","Cuprizone","Demyelinating Diseases","Disease Models, Animal","Humans","Immunohistochemistry","In Situ Nick-End Labeling","Macrophages","Male","Mice","Mice, Knockout","Microglia","Monoamine Oxidase Inhibitors","Myelin Sheath","Oligodendroglia","Receptors, Tumor Necrosis Factor","Receptors, Tumor Necrosis Factor, Type I","Receptors, Tumor Necrosis Factor, Type II","Stem Cells","Tumor Necrosis Factor-alpha","Up-Regulation"],"mesh_terms":["Animals","B-Lymphocytes","Brain Chemistry","Corpus Callosum","Cuprizone","Demyelinating Diseases","Disease Models, Animal","Humans","Immunohistochemistry","Macrophages","Male","Monoamine Oxidase Inhibitors","Myelin Sheath","Oligodendroglia","Stem Cells","Tumor Necrosis Factor-alpha","Antigens, CD","Up-Regulation","Apoptosis","Microglia","Receptors, Tumor Necrosis Factor","Mice, Knockout","In Situ Nick-End Labeling","Receptors, Tumor Necrosis Factor, Type I","Receptors, Tumor Necrosis Factor, Type II","Mice"],"keywords":["Remyelination","Oligodendrocyte","Myelin","Biology","Regeneration (biology)","Progenitor cell","Tumor necrosis factor alpha","Cell biology","Bromodeoxyuridine","Neuroscience","Immunology","Immunohistochemistry","Stem cell","Central nervous system","Brain Chemistry","Male","Mice, Knockout","B-Lymphocytes","Monoamine Oxidase Inhibitors","Macrophages","Apoptosis","Corpus Callosum","Cuprizone","Disease Models, Animal","Mice","Oligodendroglia","Antigens, CD","In Situ Nick-End Labeling","Animals","Humans","Microglia","Myelin Sheath","Demyelinating Diseases"],"sdg_mappings":[{"sdg_number":0,"sdg_label":"Good health and well-being"}],"linked_datasets":[{"doi":"10.6084/m9.figshare.13551903.v1","title":"Additional file 1 of Neuroinflammatory processes are augmented in 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