Hosang, Leon

[["dc.bibliographiccitation.artnumber","14241"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Berghoff, Stefan A."],["dc.contributor.author","Gerndt, Nina"],["dc.contributor.author","Winchenbach, Jan"],["dc.contributor.author","Stumpf, Sina Kristin"],["dc.contributor.author","Hosang, Leon"],["dc.contributor.author","Odoardi, Francesca"],["dc.contributor.author","Ruhwedel, Torben"],["dc.contributor.author","Boehler, Carolin"],["dc.contributor.author","Barrette, Benoit"],["dc.contributor.author","Stassart, Ruth"],["dc.contributor.author","Liebetanz, David"],["dc.contributor.author","Dibaj, Payam"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Edgar, Julia M."],["dc.contributor.author","Saher, Gesine"],["dc.date.accessioned","2018-11-07T10:28:16Z"],["dc.date.available","2018-11-07T10:28:16Z"],["dc.date.issued","2017"],["dc.description.abstract","Multiple Sclerosis (MS) is an inflammatory demyelinating disorder in which remyelination failure contributes to persistent disability. Cholesterol is rate-limiting for myelin biogenesis in the developing CNS; however, whether cholesterol insufficiency contributes to remyelination failure in MS, is unclear. Here, we show the relationship between cholesterol, myelination and neurological parameters in mouse models of demyelination and remyelination. In the cuprizone model, acute disease reduces serum cholesterol levels that can be restored by dietary cholesterol. Concomitant with blood-brain barrier impairment, supplemented cholesterol directly supports oligodendrocyte precursor proliferation and differentiation, and restores the balance of growth factors, creating a permissive environment for repair. This leads to attenuated axon damage, enhanced remyelination and improved motor learning. Remarkably, in experimental autoimmune encephalomyelitis, cholesterol supplementation does not exacerbate disease expression. These findings emphasize the safety of dietary cholesterol in inflammatory diseases and point to a previously unrecognized role of cholesterol in promoting repair after demyelinating episodes."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [SA 2014/2-1]; ERC Advanced grant"],["dc.identifier.doi","10.1038/ncomms14241"],["dc.identifier.isi","000392582700001"],["dc.identifier.pmid","28117328"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14258"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43386"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","2041-1723"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Dietary cholesterol promotes repair of demyelinated lesions in the adult brain"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e2006838"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","PLOS Biology"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Favaro, Plinio D."],["dc.contributor.author","Huang, Xiaojie"],["dc.contributor.author","Hosang, Leon"],["dc.contributor.author","Stodieck, Sophia"],["dc.contributor.author","Cui, Lei"],["dc.contributor.author","Liu, Yu-Zhang"],["dc.contributor.author","Engelhardt, Karl-Alexander"],["dc.contributor.author","Schmitz, Frank"],["dc.contributor.author","Dong, Yan"],["dc.contributor.author","Löwel, Siegrid"],["dc.contributor.author","Schlüter, Oliver M."],["dc.date.accessioned","2019-07-09T11:49:59Z"],["dc.date.available","2019-07-09T11:49:59Z"],["dc.date.issued","2018"],["dc.description.abstract","The disc-large (DLG)-membrane-associated guanylate kinase (MAGUK) family of proteins forms a central signaling hub of the glutamate receptor complex. Among this family, some proteins regulate developmental maturation of glutamatergic synapses, a process vulnerable to aberrations, which may lead to neurodevelopmental disorders. As is typical for paralogs, the DLG-MAGUK proteins postsynaptic density (PSD)-95 and PSD-93 share similar functional domains and were previously thought to regulate glutamatergic synapses similarly. Here, we show that they play opposing roles in glutamatergic synapse maturation. Specifically, PSD-95 promoted, whereas PSD-93 inhibited maturation of immature α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid-type glutamate receptor (AMPAR)-silent synapses in mouse cortex during development. Furthermore, through experience-dependent regulation of its protein levels, PSD-93 directly inhibited PSD-95's promoting effect on silent synapse maturation in the visual cortex. The concerted function of these two paralogs governed the critical period of juvenile ocular dominance plasticity (jODP), and fine-tuned visual perception during development. In contrast to the silent synapse-based mechanism of adjusting visual perception, visual acuity improved by different mechanisms. Thus, by controlling the pace of silent synapse maturation, the opposing but properly balanced actions of PSD-93 and PSD-95 are essential for fine-tuning cortical networks for receptive field integration during developmental critical periods, and imply aberrations in either direction of this process as potential causes for neurodevelopmental disorders."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2018"],["dc.identifier.doi","10.1371/journal.pbio.2006838"],["dc.identifier.pmid","30586380"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15797"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15829"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59674"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1545-7885"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.subject.ddc","612"],["dc.title","An opposing function of paralogs in balancing developmental synapse maturation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]