Ribas, Vinicius Toledo

[["dc.bibliographiccitation.firstpage","72"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Molecular Neurobiology"],["dc.bibliographiccitation.lastpage","86"],["dc.bibliographiccitation.volume","54"],["dc.contributor.author","Ribas, Vinicius Toledo"],["dc.contributor.author","Koch, Jan C."],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2018-01-09T11:14:21Z"],["dc.date.available","2018-01-09T11:14:21Z"],["dc.date.issued","2017"],["dc.description.abstract","Axonal degeneration is one of the initial steps in many traumatic and neurodegenerative central nervous system (CNS) disorders and thus a promising therapeutic target. A focal axonal lesion is followed by acute axonal degeneration (AAD) of both adjacent axon parts, before proximal and distal parts follow different degenerative fates at later time points. Blocking calcium influx by calcium channel inhibitors was previously shown to attenuate AAD after optic nerve crush (ONC). However, it remains unclear whether the attenuation of AAD also promotes consecutive axonal regeneration. Here, we used a rat ONC model to study the effects of calcium channel inhibitors on axonal degeneration, retinal ganglion cell (RGC) survival, and axonal regeneration, as well as the molecular mechanisms involved. Application of calcium channel inhibitors attenuated AAD after ONC and preserved axonal integrity as visualized by live imaging of optic nerve axons. Consecutively, this resulted in improved survival of RGCs and improved axonal regeneration at 28 days after ONC. We show further that calcium channel inhibition attenuated lesion-induced calpain activation in the proximity of the crush and inhibited the activation of the c-Jun N-terminal kinase pathway. Pro-survival signaling via Akt in the retina was also increased. Our data thus show that attenuation of AAD improves consecutive neuronal survival and axonal regeneration and that calcium channel inhibitors could be valuable tools for therapeutic interventions in traumatic and degenerative CNS disorders."],["dc.identifier.doi","10.1007/s12035-015-9676-2"],["dc.identifier.pmid","26732591"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11580"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1559-1182"],["dc.title","Attenuation of Axonal Degeneration by Calcium Channel Inhibitors Improves Retinal Ganglion Cell Survival and Regeneration After Optic Nerve Crush"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","685"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Molecular Neurobiology"],["dc.bibliographiccitation.lastpage","697"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Balke, Dirk"],["dc.contributor.author","Tatenhorst, Lars"],["dc.contributor.author","Dambeck, Vivian"],["dc.contributor.author","Ribas, Vinicius Toledo"],["dc.contributor.author","Vahsen, Björn F."],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2020-12-10T14:14:28Z"],["dc.date.available","2020-12-10T14:14:28Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1007/s12035-019-01744-0"],["dc.identifier.eissn","1559-1182"],["dc.identifier.issn","0893-7648"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71353"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","AAV-Mediated Expression of Dominant-Negative ULK1 Increases Neuronal Survival and Enhances Motor Performance in the MPTP Mouse Model of Parkinson’s Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2810"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Cell Death and Differentiation"],["dc.bibliographiccitation.lastpage","2827"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Vahsen, Björn Friedhelm"],["dc.contributor.author","Ribas, Vinicius Toledo"],["dc.contributor.author","Sundermeyer, Jonas"],["dc.contributor.author","Boecker, Alexander"],["dc.contributor.author","Dambeck, Vivian"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Shomroni, Orr"],["dc.contributor.author","Caldi Gomes, Lucas"],["dc.contributor.author","Tatenhorst, Lars"],["dc.contributor.author","Barski, Elisabeth"],["dc.contributor.author","Roser, Anna-Elisa"],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Salinas, Gabriela"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Koch, Jan Christoph"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2020-12-10T18:09:42Z"],["dc.date.available","2020-12-10T18:09:42Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1038/s41418-020-0543-y"],["dc.identifier.eissn","1476-5403"],["dc.identifier.issn","1350-9047"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73733"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Inhibition of the autophagic protein ULK1 attenuates axonal degeneration in vitro and in vivo, enhances translation, and modulates splicing"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","261"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","275"],["dc.bibliographiccitation.volume","134"],["dc.contributor.author","Challagundla, Malleswari"],["dc.contributor.author","Koch, Jan Christoph"],["dc.contributor.author","Ribas, Vinicius Toledo"],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Kügler, Sebastian"],["dc.contributor.author","Ostendorf, Thomas"],["dc.contributor.author","Bradke, Frank"],["dc.contributor.author","Müller, H. W."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2017-09-07T11:43:44Z"],["dc.date.available","2017-09-07T11:43:44Z"],["dc.date.issued","2015"],["dc.description.abstract","A lesion to the rat rubrospinal tract is a model for traumatic spinal cord lesions and results in atrophy of the red nucleus neurons, axonal dieback, and locomotor deficits. In this study, we used adeno-associated virus (AAV)-mediated over-expression of BAG1 and ROCK2-shRNA in the red nucleus to trace [by co-expression of enhanced green fluorescent protein (EGFP)] and treat the rubrospinal tract after unilateral dorsal hemisection. We investigated the effects of targeted gene therapy on neuronal survival, axonal sprouting of the rubrospinal tract, and motor recovery 12weeks after unilateral dorsal hemisection at Th-8 in rats. In addition to the evaluation of BAG1 and ROCK2 as therapeutic targets in spinal cord injury, we aimed to demonstrate the feasibility and the limits of an AAV-mediated protein over-expression versus AAV.shRNA-mediated down-regulation in this traumatic CNS lesion model. Our results demonstrate that BAG1 and ROCK2-shRNA both promote neuronal survival of red nucleus neurons and enhance axonal sprouting proximal to the lesion."],["dc.identifier.doi","10.1111/jnc.13102"],["dc.identifier.gro","3141874"],["dc.identifier.isi","000357598000008"],["dc.identifier.pmid","25807858"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2034"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1471-4159"],["dc.relation.issn","0022-3042"],["dc.title","AAV-mediated expression of BAG1 and ROCK2-shRNA promote neuronal survival and axonal sprouting in a rat model of rubrospinal tract injury"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cell Death & Disease"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Ribas, Vinicius Toledo"],["dc.contributor.author","Vahsen, Björn Friedhelm"],["dc.contributor.author","Tatenhorst, Lars"],["dc.contributor.author","Estrada, Veronica"],["dc.contributor.author","Dambeck, Vivian"],["dc.contributor.author","Almeida, Raquel Alves"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Koch, Jan Christoph"],["dc.contributor.author","Müller, Hans Werner"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2021-04-14T08:28:39Z"],["dc.date.available","2021-04-14T08:28:39Z"],["dc.date.issued","2021"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.1038/s41419-021-03503-3"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82673"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","2041-4889"],["dc.relation.orgunit","Abteilung Neurobiologie"],["dc.rights","CC BY 4.0"],["dc.title","AAV-mediated inhibition of ULK1 promotes axonal regeneration in the central nervous system in vitro and in vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","150"],["dc.bibliographiccitation.journal","Neurobiology of Disease"],["dc.bibliographiccitation.lastpage","162"],["dc.bibliographiccitation.volume","73"],["dc.contributor.author","Saal, K.-A."],["dc.contributor.author","Koch, J. C."],["dc.contributor.author","Tatenhorst, L."],["dc.contributor.author","Szegő, É. M."],["dc.contributor.author","Ribas, V. T."],["dc.contributor.author","Michel, U."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Tönges, L."],["dc.contributor.author","Lingor, P."],["dc.date.accessioned","2017-09-07T11:45:21Z"],["dc.date.available","2017-09-07T11:45:21Z"],["dc.date.issued","2015"],["dc.description.abstract","Parkinson's disease (PD) is a neurodegenerative disorder with prominent neuronal cell death in the substantia nigra (SN) and other parts of the brain. Previous studies in models of traumatic and neurodegenerative CNS disease showed that pharmacological inhibition of Rho-associated kinase (ROCK), a molecule involved in inhibitory signaling in the CNS, by small-molecule inhibitors improves neuronal survival and increases regeneration. Most small-molecule inhibitors, however, offer only limited target specificity and also inhibit other kinases, including both ROCK isoforms. To establish the role of the predominantly brain-expressed ROCK2 isoform in models of regeneration and PD, we used adeno-associated viral vectors (MV) to specifically knockdown ROCK2 in neurons. Rat primary midbrain neurons (PMN) were transduced with MV expressing short-hairpin-RNA (shRNA) against ROCK2 and LIM-domain kinase 1 (LIMK1), one of the downstream targets of ROCK2. While knock-down of ROCK2 and LIMK1 both enhanced neurite regeneration in a traumatic scratch lesion model, only ROCK2-shRNA protected PMN against 1-methyl-4-phenylpyridinium (MPP+) toxicity. Moreover, AAV.ROCK2-shRNA increased levels of the pro-survival markers Bcl-2 and phospho-Erk1. In vivo, AAV.ROCK2-shRNA vectors were injected into the ipsilateral SN and a unilateral 6-OHDA striatal lesion was performed. After four weeks, behavioral, immunohistochemical and biochemical alterations were investigated. Downregulation of ROCK2 protected dopaminergic neurons in the SN from 6-OHDA-induced degeneration and resulted in significantly increased TH-positive neuron numbers. This effect, however, was confined to nigral neuronal somata as striatal terminal density, dopamine and metabolite levels were not significantly preserved. Interestingly, motor behavior was improved in the ROCK2-shRNA treated animals compared to control after four weeks. Our studies thus confirm ROCK2 as a promising therapeutic target in models of PD and demonstrate that neuronspecific inhibition of ROCK2 promotes survival of lesioned dopaminergic neurons. (C) 2015 Elsevier Inc All rights reserved."],["dc.identifier.doi","10.1016/j.nbd.2014.09.013"],["dc.identifier.gro","3141993"],["dc.identifier.isi","000346328100014"],["dc.identifier.pmid","25283984"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/3357"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1095-953X"],["dc.relation.issn","0969-9961"],["dc.title","AAV.shRNA-mediated downregulation of ROCK2 attenuates degeneration of dopaminergic neurons in toxin-induced models of Parkinson's disease in vitro and in vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]