Döppner, Thorsten Roland

[["dc.bibliographiccitation.firstpage","328"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Aging"],["dc.bibliographiccitation.lastpage","349"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Jin, Fengyan"],["dc.contributor.author","Zheng, Xiangyu"],["dc.contributor.author","Yang, Yanping"],["dc.contributor.author","Yao, Gang"],["dc.contributor.author","Ye, Long"],["dc.contributor.author","Doeppner, Thorsten R."],["dc.contributor.author","Hermann, Dirk M."],["dc.contributor.author","Wang, Haifeng"],["dc.contributor.author","Dai, Yun"],["dc.date.accessioned","2020-12-10T18:42:50Z"],["dc.date.available","2020-12-10T18:42:50Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.18632/aging.v11i2"],["dc.identifier.eissn","1945-4589"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78102"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Impairment of hypoxia-induced angiogenesis by LDL involves a HIF-centered signaling network linking inflammatory TNFα and angiogenic VEGF"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2044"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","STEM CELLS Translational Medicine"],["dc.bibliographiccitation.lastpage","2052"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Doeppner, Thorsten R."],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Hermann, Dirk M."],["dc.contributor.author","Giebel, Bernd"],["dc.date.accessioned","2018-04-23T11:49:28Z"],["dc.date.available","2018-04-23T11:49:28Z"],["dc.date.issued","2017"],["dc.description.abstract","Despite recent advances in stroke therapy, current therapeutic concepts are still limited. Thus, additional therapeutic strategies are in order. In this sense, the transplantation of stem cells has appeared to be an attractive adjuvant tool to help boost the endogenous regenerative capacities of the brain. Although transplantation of stem cells is known to induce beneficial outcome in (preclinical) stroke research, grafted cells do not replace lost tissue directly. Rather, these transplanted cells like neural progenitor cells or mesenchymal stem cells act in an indirect manner, among which the secretion of extracellular vesicles (EVs) appears to be one key factor. Indeed, the application of EVs in preclinical stroke studies suggests a therapeutic role, which appears to be noninferior in comparison to the transplantation of stem cells themselves. In this short review, we highlight some of the recent advances in the field of EVs as a therapeutic means to counter stroke."],["dc.identifier.doi","10.1002/sctm.17-0081"],["dc.identifier.gro","3142068"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13702"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.status","final"],["dc.relation.issn","2157-6564"],["dc.title","Concise Review: Extracellular Vesicles Overcoming Limitations of Cell Therapies in Ischemic Stroke"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","102989"],["dc.bibliographiccitation.journal","EBioMedicine"],["dc.bibliographiccitation.volume","60"],["dc.contributor.author","Danielyan, Lusine"],["dc.contributor.author","Schwab, Matthias"],["dc.contributor.author","Siegel, Georg"],["dc.contributor.author","Brawek, Bianca"],["dc.contributor.author","Garaschuk, Olga"],["dc.contributor.author","Asavapanumas, Nithi"],["dc.contributor.author","Buadze, Marine"],["dc.contributor.author","Lourhmati, Ali"],["dc.contributor.author","Wendel, Hans-Peter"],["dc.contributor.author","Avci-Adali, Meltem"],["dc.contributor.author","Krueger, Marcel A."],["dc.contributor.author","Calaminus, Carsten"],["dc.contributor.author","Naumann, Ulrike"],["dc.contributor.author","Winter, Stefan"],["dc.contributor.author","Schaeffeler, Elke"],["dc.contributor.author","Spogis, Annett"],["dc.contributor.author","Beer-Hammer, Sandra"],["dc.contributor.author","Neher, Jonas J."],["dc.contributor.author","Spohn, Gabriele"],["dc.contributor.author","Kretschmer, Anja"],["dc.contributor.author","Krämer-Albers, Eva-Maria"],["dc.contributor.author","Barth, Kerstin"],["dc.contributor.author","Lee, Hong Jun"],["dc.contributor.author","Kim, Seung U."],["dc.contributor.author","Frey, William H."],["dc.contributor.author","Claussen, Claus D."],["dc.contributor.author","Hermann, Dirk M."],["dc.contributor.author","Doeppner, Thorsten R."],["dc.contributor.author","Seifried, Erhard"],["dc.contributor.author","Gleiter, Christoph H."],["dc.contributor.author","Northoff, Hinnak"],["dc.contributor.author","Schäfer, Richard"],["dc.date.accessioned","2021-04-14T08:23:30Z"],["dc.date.available","2021-04-14T08:23:30Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1016/j.ebiom.2020.102989"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/80939"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.issn","2352-3964"],["dc.title","Cell motility and migration as determinants of stem cell efficacy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","114442"],["dc.bibliographiccitation.issue","70"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","114456"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Wang, Xue"],["dc.contributor.author","Wang, Siqing"],["dc.contributor.author","Yao, Gang"],["dc.contributor.author","Yu, Dehai"],["dc.contributor.author","Chen, Kexin"],["dc.contributor.author","Tong, Qian"],["dc.contributor.author","Ye, Long"],["dc.contributor.author","Wu, Chuan"],["dc.contributor.author","Sun, Yue"],["dc.contributor.author","Li, Haixia"],["dc.contributor.author","Hermann, Dirk M."],["dc.contributor.author","Doeppner, Thorsten R."],["dc.contributor.author","Jin, Fengyan"],["dc.contributor.author","Dai, Yun"],["dc.contributor.author","Wu, Jiang"],["dc.date.accessioned","2020-12-10T18:42:50Z"],["dc.date.available","2020-12-10T18:42:50Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.18632/oncotarget.v8i70"],["dc.identifier.eissn","1949-2553"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78106"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Identification of the histone lysine demethylase KDM4A/JMJD2A as a novel epigenetic target in M1 macrophage polarization induced by oxidized LDL"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","102987"],["dc.bibliographiccitation.journal","EBioMedicine"],["dc.bibliographiccitation.volume","60"],["dc.contributor.author","Schäfer, Richard"],["dc.contributor.author","Schwab, Matthias"],["dc.contributor.author","Siegel, Georg"],["dc.contributor.author","von Ameln-Mayerhofer, Andreas"],["dc.contributor.author","Buadze, Marine"],["dc.contributor.author","Lourhmati, Ali"],["dc.contributor.author","Wendel, Hans-Peter"],["dc.contributor.author","Kluba, Torsten"],["dc.contributor.author","Krueger, Marcel A."],["dc.contributor.author","Calaminus, Carsten"],["dc.contributor.author","Scheer, Eva"],["dc.contributor.author","Dominici, Massimo"],["dc.contributor.author","Grisendi, Giulia"],["dc.contributor.author","Doeppner, Thorsten R."],["dc.contributor.author","Schlechter, Jana"],["dc.contributor.author","Finzel, Anne Kathrin"],["dc.contributor.author","Gross, Dominic"],["dc.contributor.author","Klaffschenkel, Roland"],["dc.contributor.author","Gehring, Frank K."],["dc.contributor.author","Spohn, Gabriele"],["dc.contributor.author","Kretschmer, Anja"],["dc.contributor.author","Bieback, Karen"],["dc.contributor.author","Krämer-Albers, Eva-Maria"],["dc.contributor.author","Barth, Kerstin"],["dc.contributor.author","Eckert, Anne"],["dc.contributor.author","Elser, Stefanie"],["dc.contributor.author","Schmehl, Joerg"],["dc.contributor.author","Claussen, Claus D."],["dc.contributor.author","Seifried, Erhard"],["dc.contributor.author","Hermann, Dirk M."],["dc.contributor.author","Northoff, Hinnak"],["dc.contributor.author","Danielyan, Lusine"],["dc.date.accessioned","2021-04-14T08:23:30Z"],["dc.date.available","2021-04-14T08:23:30Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1016/j.ebiom.2020.102987"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/80940"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.issn","2352-3964"],["dc.title","Modulating endothelial adhesion and migration impacts stem cell therapies efficacy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3348"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Stroke"],["dc.bibliographiccitation.lastpage","3350"],["dc.bibliographiccitation.volume","52"],["dc.contributor.author","Hermann, Dirk M."],["dc.contributor.author","Doeppner, Thorsten R."],["dc.contributor.author","Giebel, Bernd"],["dc.date.accessioned","2021-12-01T09:23:58Z"],["dc.date.available","2021-12-01T09:23:58Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1161/STROKEAHA.121.036150"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94808"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","1524-4628"],["dc.relation.issn","0039-2499"],["dc.title","New Light on the Horizon"],["dc.title.alternative","Extracellular Vesicles as Diagnostic Tool in Transient Ischemic Attack and Ischemic Stroke"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","6061"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Molecular neurobiology"],["dc.bibliographiccitation.lastpage","6073"],["dc.bibliographiccitation.volume","54"],["dc.contributor.author","Doeppner, Thorsten R."],["dc.contributor.author","Doehring, Maria"],["dc.contributor.author","Kaltwasser, Britta"],["dc.contributor.author","Majid, Arshad"],["dc.contributor.author","Lin, Fengyan"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Kilic, Ertugrul"],["dc.contributor.author","Hermann, Dirk M."],["dc.date.accessioned","2018-01-08T16:54:34Z"],["dc.date.available","2018-01-08T16:54:34Z"],["dc.date.issued","2017"],["dc.description.abstract","In view of the failure of pharmacological therapies, alternative strategies promoting post-stroke brain repair are needed. Post-conditioning is a potentially promising therapeutic strategy, which induces acute neuroprotection against ischemic injury. To elucidate longer lasting actions of ischemic post-conditioning, mice were exposed to a 60-min stroke and post-conditioning by an additional 10-min stroke that was induced 10 min after reperfusion onset. Animals were sacrificed 24 h or 28 days post-stroke. Post-conditioning reduced infarct volume and neurological deficits 24 h post-stroke, enhancing blood-brain barrier integrity, reducing brain leukocyte infiltration, and reducing oxidative stress. On the molecular level, post-conditioning yielded increased Hsp70 expression, whereas nuclear factor (NF)-κB and proteasome activities were decreased. Reduced infarct volume and proteasome inhibition were reversed by Hsp70 knockdown, suggesting a critical role of the Hsp70 proteasome pathway in ischemic post-conditioning. The survival-promoting effects of ischemic post-conditioning, however, were not sustainable as neuroprotection and neurological recovery were lost 28 days post-stroke. Although angioneurogenesis was not increased by post-conditioning, the favorable extracellular milieu facilitated intracerebral transplantation of neural progenitor cells 6 h post-stroke, resulting in persisted neuroprotection and neurological recovery. Thus, post-conditioning might support brain repair processes, but in view of its transient, neuroprotection is unlikely useful as stroke therapy in its current form."],["dc.identifier.doi","10.1007/s12035-016-0137-3"],["dc.identifier.pmid","27699598"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11571"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1559-1182"],["dc.title","Ischemic Post-Conditioning Induces Post-Stroke Neuroprotection via Hsp70-Mediated Proteasome Inhibition and Facilitates Neural Progenitor Cell Transplantation"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0177069"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Sanchez-Mendoza, Eduardo H."],["dc.contributor.author","Bellver-Landete, Victor"],["dc.contributor.author","Arce, Carmen"],["dc.contributor.author","Doeppner, Thorsten R."],["dc.contributor.author","Hermann, Dirk M."],["dc.contributor.author","Jesus Oset-Gasque, Maria"],["dc.date.accessioned","2018-11-07T10:23:51Z"],["dc.date.available","2018-11-07T10:23:51Z"],["dc.date.issued","2017"],["dc.description.abstract","The role of glutamate in the regulation of neurogenesis is well-established, but the role of vesicular glutamate transporters (VGLUTs) and excitatory amino acid transporters (EAATs) in controlling adult neurogenesis is unknown. Here we investigated the implication of VGLUTs in the differentiation of subventricular zone (SVZ)-derived neural precursor cells (NPCs). Our results show that NPCs express VGLUT1-3 and EAAT1-3 both at the mRNA and protein level. Their expression increases during differentiation closely associated with the expression of marker genes. In expression analyses we show that VGLUT1 and VGLUT2 are preferentially expressed by cultured SVZ-derived doublecortin+ neuroblasts, while VGLUT3 is found on GFAP+ glial cells. In cultured NPCs, inhibition of VGLUT by Evans Blue increased the mRNA level of neuronal markers doublecortin, B3T and MAP2, elevated the number of NPCs expressing doublecortin protein and promoted the number of cells with morphological appearance of branched neurons, suggesting that VGLUT function prevents neuronal differentiation of NPCs. This survival-and differentiation-promoting effect of Evans blue was corroborated by increased AKT phosphorylation and reduced MAPK phosphorylation. Thus, under physiological conditions, VGLUT1-3 inhibition, and thus decreased glutamate exocytosis, may promote neuronal differentiation of NPCs."],["dc.identifier.doi","10.1371/journal.pone.0177069"],["dc.identifier.isi","000401314300056"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14489"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42540"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Vesicular glutamate transporters play a role in neuronal differentiation of cultured SVZ-derived neural precursor cells"],["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.firstpage","914"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Cerebral Blood Flow & Metabolism"],["dc.bibliographiccitation.lastpage","926"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Kaltwasser, Britta"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Doeppner, Thorsten R."],["dc.contributor.author","Sanchez-Mendoza, Eduardo H."],["dc.contributor.author","Caglayan, Ahmet B."],["dc.contributor.author","Hermann, Dirk M."],["dc.date.accessioned","2020-12-10T18:38:25Z"],["dc.date.available","2020-12-10T18:38:25Z"],["dc.date.issued","2016"],["dc.description.abstract","Lithium promotes acute poststroke neuronal survival, which includes mechanisms that are not limited to GSK3β inhibition. However, whether lithium induces long-term neuroprotection and enhanced brain remodeling is unclear. Therefore, mice were exposed to transient middle cerebral artery occlusion and lithium (1 mg/kg bolus followed by 2 mg/kg/day over up to 7 days) was intraperitoneally administered starting 0-9 h after reperfusion onset. Delivery of lithium no later than 6 h reduced infarct volume on day 2 and decreased brain edema, leukocyte infiltration, and microglial activation, as shown by histochemistry and flow cytometry. Lithium-induced neuroprotection persisted throughout the observation period of 56 days and was associated with enhanced neurological recovery. Poststroke angioneurogenesis and axonal plasticity were also enhanced by lithium. On the molecular level, lithium increased miR-124 expression, reduced RE1-silencing transcription factor abundance, and decreased protein deubiquitination in cultivated cortical neurons exposed to oxygen-glucose deprivation and in brains of mice exposed to cerebral ischemia. Notably, this effect was not mimicked by pharmacological GSK3β inhibition. This study for the first time provides efficacy data for lithium in the postacute ischemic phase, reporting a novel mechanism of action, i.e. increased miR-124 expression facilitating REST degradation by which lithium promotes postischemic neuroplasticity and angiogenesis."],["dc.identifier.doi","10.1177/0271678X16647738"],["dc.identifier.eissn","1559-7016"],["dc.identifier.issn","0271-678X"],["dc.identifier.pmid","27126323"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77307"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.status","final"],["dc.relation.eissn","1559-7016"],["dc.title","Lithium-induced neuroprotection in stroke involves increased miR-124 expression, reduced RE1-silencing transcription factor abundance and decreased protein deubiquitination by GSK3β inhibition-independent pathways"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","954"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Stroke"],["dc.bibliographiccitation.lastpage","956"],["dc.bibliographiccitation.volume","52"],["dc.contributor.author","Hermann, Dirk M."],["dc.contributor.author","Doeppner, Thorsten R."],["dc.contributor.author","Giebel, Bernd"],["dc.date.accessioned","2021-06-01T09:42:12Z"],["dc.date.available","2021-06-01T09:42:12Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1161/STROKEAHA.120.033688"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85176"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1524-4628"],["dc.relation.issn","0039-2499"],["dc.title","Circulating MicroRNAs"],["dc.title.alternative","Posttranscriptional Regulators and Disease Markers Holding Promise in Stroke Prediction"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]