{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1360572092373157248.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1038/s41419-021-03469-2"}},{"identifier":{"@type":"URI","@value":"https://www.nature.com/articles/s41419-021-03469-2.pdf"}},{"identifier":{"@type":"URI","@value":"https://www.nature.com/articles/s41419-021-03469-2"}},{"identifier":{"@type":"PMID","@value":"33589594"}}],"resourceType":"学術雑誌論文(journal article)","dc:title":[{"@value":"Inhibition of repulsive guidance molecule-a protects dopaminergic neurons in a mouse model of Parkinson’s disease"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:title>Abstract</jats:title><jats:p>Repulsive guidance molecule-a (RGMa), a glycosylphosphatidylinositol-anchored membrane protein, has diverse functions in axon guidance, cell patterning, and cell survival. Inhibition of RGMa attenuates pathological dysfunction in animal models of central nervous system (CNS) diseases including spinal cord injury, multiple sclerosis, and neuromyelitis optica. Here, we examined whether antibody-based inhibition of RGMa had therapeutic effects in a mouse model of Parkinson’s disease (PD). We treated mice with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and found increased RGMa expression in the substantia nigra (SN). Intraventricular, as well as intravenous, administration of anti-RGMa antibodies reduced the loss of tyrosine hydroxylase (TH)-positive neurons and accumulation of Iba1-positive microglia/macrophages in the SN of MPTP-treated mice. Selective expression of RGMa in TH-positive neurons in the SN-induced neuronal loss/degeneration and inflammation, resulting in a progressive movement disorder. The pathogenic effects of RGMa overexpression were attenuated by treatment with minocycline, which inhibits microglia and macrophage activation. Increased RGMa expression upregulated pro-inflammatory cytokine expression in microglia. Our observations suggest that the upregulation of RGMa is associated with the PD pathology; furthermore, inhibitory RGMa antibodies are a potential therapeutic option.</jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1380572092373157003","@type":"Researcher","foaf:name":[{"@value":"Wakana Oda"}]},{"@id":"https://cir.nii.ac.jp/crid/1380572092373157001","@type":"Researcher","foaf:name":[{"@value":"Yuki Fujita"}]},{"@id":"https://cir.nii.ac.jp/crid/1420282801214261504","@type":"Researcher","personIdentifier":[{"@type":"KAKEN_RESEARCHERS","@value":"90750159"},{"@type":"NRID","@value":"1000090750159"},{"@type":"NRID","@value":"9000327092214"},{"@type":"NRID","@value":"9000411101159"},{"@type":"NRID","@value":"9000345264288"},{"@type":"NRID","@value":"9000273397129"},{"@type":"RESEARCHMAP","@value":"https://researchmap.jp/5017"}],"foaf:name":[{"@value":"Kousuke Baba"}]},{"@id":"https://cir.nii.ac.jp/crid/1380572092373157002","@type":"Researcher","foaf:name":[{"@value":"Hideki Mochizuki"}]},{"@id":"https://cir.nii.ac.jp/crid/1380572092373157252","@type":"Researcher","foaf:name":[{"@value":"Hitoshi Niwa"}]},{"@id":"https://cir.nii.ac.jp/crid/1420845751158287360","@type":"Researcher","personIdentifier":[{"@type":"KAKEN_RESEARCHERS","@value":"10301269"},{"@type":"NRID","@value":"1000010301269"},{"@type":"ORCID","@value":"0000-0003-4559-7018"},{"@type":"NRID","@value":"9000276152205"},{"@type":"NRID","@value":"9000324643534"},{"@type":"NRID","@value":"9000341541214"},{"@type":"NRID","@value":"9000282424057"},{"@type":"NRID","@value":"9000399182819"},{"@type":"NRID","@value":"9000324642477"},{"@type":"NRID","@value":"9000398383959"},{"@type":"NRID","@value":"9000001829363"},{"@type":"NRID","@value":"9000380123835"},{"@type":"NRID","@value":"9000341541225"},{"@type":"NRID","@value":"9000257959183"},{"@type":"NRID","@value":"9000324985096"},{"@type":"NRID","@value":"9000242119044"},{"@type":"NRID","@value":"9000356609964"},{"@type":"NRID","@value":"9000018468757"},{"@type":"RESEARCHMAP","@value":"https://researchmap.jp/ToshihideYamashita"}],"foaf:name":[{"@value":"Toshihide Yamashita"}]}],"publication":{"publicationIdentifier":[{"@type":"EISSN","@value":"20414889"}],"prism:publicationName":[{"@value":"Cell Death & Disease"}],"dc:publisher":[{"@value":"Springer Science and Business Media LLC"}],"prism:publicationDate":"2021-02-15","prism:volume":"12","prism:number":"2","prism:startingPage":"181"},"reviewed":"false","dcterms:accessRights":"http://purl.org/coar/access_right/c_abf2","dc:rights":["https://creativecommons.org/licenses/by/4.0","https://creativecommons.org/licenses/by/4.0"],"url":[{"@id":"https://www.nature.com/articles/s41419-021-03469-2.pdf"},{"@id":"https://www.nature.com/articles/s41419-021-03469-2"}],"createdAt":"2021-02-17","modifiedAt":"2022-12-01","foaf:topic":[{"@id":"https://cir.nii.ac.jp/all?q=Male","dc:title":"Male"},{"@id":"https://cir.nii.ac.jp/all?q=Disease%20Models,%20Animal","dc:title":"Disease Models, Animal"},{"@id":"https://cir.nii.ac.jp/all?q=Mice","dc:title":"Mice"},{"@id":"https://cir.nii.ac.jp/all?q=QH573-671","dc:title":"QH573-671"},{"@id":"https://cir.nii.ac.jp/all?q=Dopaminergic%20Neurons","dc:title":"Dopaminergic Neurons"},{"@id":"https://cir.nii.ac.jp/all?q=Animals","dc:title":"Animals"},{"@id":"https://cir.nii.ac.jp/all?q=Parkinson%20Disease","dc:title":"Parkinson Disease"},{"@id":"https://cir.nii.ac.jp/all?q=Cytology","dc:title":"Cytology"}],"project":[{"@id":"https://cir.nii.ac.jp/crid/1040000781959411328","@type":"Project","projectIdentifier":[{"@type":"KAKEN","@value":"17H06178"},{"@type":"JGN","@value":"JP17H06178"},{"@type":"URI","@value":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-17H06178/"}],"notation":[{"@language":"ja","@value":"神経回路修復医学の創成"},{"@language":"en","@value":"Generation of neural network repair medicine"}]}],"relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1050581168899417600","@type":"Article","resourceType":"学術雑誌論文(journal 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Disease"}]},{"@id":"https://cir.nii.ac.jp/crid/1363670318988903168","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Activated Microglia Inhibit Axonal Growth through RGMa"}]},{"@id":"https://cir.nii.ac.jp/crid/1363670320412542080","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Some features of the nigrostriatal dopaminergic neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in the mouse"}]},{"@id":"https://cir.nii.ac.jp/crid/1363951793931891712","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Inhibition of rho kinase enhances survival of dopaminergic neurons and attenuates axonal loss in a mouse model of Parkinson's disease"}]},{"@id":"https://cir.nii.ac.jp/crid/1363951794698760960","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Neogenin, a Receptor for Bone Morphogenetic 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