Keric, Naureen

[["dc.bibliographiccitation.firstpage","1055"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Nature Medicine"],["dc.bibliographiccitation.lastpage","1061"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Fledrich, Robert"],["dc.contributor.author","Stassart, Ruth Martha"],["dc.contributor.author","Klink, Axel"],["dc.contributor.author","Rasch, Lennart M."],["dc.contributor.author","Prukop, Thomas"],["dc.contributor.author","Haag, Lauren"],["dc.contributor.author","Czesnik, Dirk"],["dc.contributor.author","Kungl, Theresa"],["dc.contributor.author","Abdelaal, Tamer A. M."],["dc.contributor.author","Keric, Naureen"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Sereda, Michael W."],["dc.date.accessioned","2018-11-07T09:36:01Z"],["dc.date.available","2018-11-07T09:36:01Z"],["dc.date.issued","2014"],["dc.description.abstract","Duplication of the gene encoding the peripheral myelin protein of 22 kDa (PMP22) underlies the most common inherited neuropathy, Charcot-Marie-Tooth 1A (CMT1A)(1-3), a disease without a known cure(4-6). Although demyelination represents a characteristic feature, the clinical phenotype of CMT1A is determined by the degree of axonal loss, and patients suffer from progressive muscle weakness and impaired sensation(4,7). CMT1A disease manifests within the first two decades of life(8,9), and walking disabilities, foot deformities and electrophysiological abnormalities are already present in childhood(7-11). Here, we show in Pmp22-transgenic rodent models of CMT1A that Schwann cells acquire a persistent differentiation defect during early postnatal development, caused by imbalanced activity of the PI3K-Akt and the Mek-Erk signaling pathways. We demonstrate that enhanced PI3K-Akt signaling by axonally overexpressed neuregulin-1 (NRG1) type I drives diseased Schwann cells toward differentiation and preserves peripheral nerve axons. Notably, in a preclinical experimental therapy using a CMT1A rat model, when treatment is restricted to early postnatal development, soluble NRG1 effectively overcomes impaired peripheral nerve development and restores axon survival into adulthood. Our findings suggest a model in which Schwann cell differentiation within a limited time window is crucial for the long-term maintenance of axonal support."],["dc.identifier.doi","10.1038/nm.3664"],["dc.identifier.isi","000341404000019"],["dc.identifier.pmid","25150498"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32517"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1546-170X"],["dc.relation.issn","1078-8956"],["dc.title","Soluble neuregulin-1 modulates disease pathogenesis in rodent models of Charcot-Marie-Tooth disease 1A"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S88"],["dc.bibliographiccitation.journal","Translational Stroke Research"],["dc.bibliographiccitation.lastpage","S93"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Keric, Naureen"],["dc.contributor.author","Maier, Gerrit Steffen"],["dc.contributor.author","Samadani, Uzma"],["dc.contributor.author","Kallenberg, Kai"],["dc.contributor.author","Dechent, Peter"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Heuer, J. F."],["dc.contributor.author","Rohde, Veit"],["dc.date.accessioned","2018-11-07T09:08:53Z"],["dc.date.available","2018-11-07T09:08:53Z"],["dc.date.issued","2012"],["dc.description.abstract","Hematoma puncture and subsequent clot lysis with recombinant tissue plasminogen activator (rtPA) emerged as an alternative therapy for spontaneous intracerebral hemorrhage (ICH) and is associated with delayed edema possibly counteracting the beneficial effects of hematoma volume reduction. We hypothesized that immediate reversal of rtPA activity after clot lysis and hematoma drainage diminishes edema formation. To test this hypothesis, we administered plasminogen activator inhibitor (PAI)-1 after rtPA lysis of experimentally induced ICH. A right frontal ICH was placed through a twist drill burr hole and autologous blood injection. Following creation of the frontal ICH, pigs received no further treatment (n=5), lysis with rtPA (n=7), or lysis with rtPA followed by administration of PAI-1 (n=6). Hematoma and edema volumes were assessed with magnetic resonance imaging on days 0, 4, and 10. The rtPA significantly reduced hematoma volume and contributed to edema on day 10 after experimentally induced ICH. Administration of PAI-1 attenuated the rtPA-induced edema volume on day 10, but the hematoma volume reduction was less pronounced. In conclusion, PAI-1 attenuated delayed cerebral edema after rtPA lysis of experimental ICH but also reduced the lytic activity of rtPA. The combination of rtPA clot lysis with PAI-1 might have the potential to further improve the effect of the lytic therapy of ICH, but additional studies to define the optimum time point for PAI-1 administration are required."],["dc.identifier.doi","10.1007/s12975-012-0188-3"],["dc.identifier.isi","000305436500011"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8890"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26132"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1868-4483"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Tissue Plasminogen Activator Induced Delayed Edema in Experimental Porcine Intracranial Hemorrhage: Reduction with Plasminogen Activator Inhibitor-1 Administration"],["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"]]