Döppner, Thorsten Roland

[["dc.bibliographiccitation.firstpage","108357"],["dc.bibliographiccitation.journal","Neuropharmacology"],["dc.bibliographiccitation.volume","181"],["dc.contributor.author","Haupt, Matteo"],["dc.contributor.author","Zechmeister, Bozena"],["dc.contributor.author","Bosche, Bert"],["dc.contributor.author","Lieschke, Simone"],["dc.contributor.author","Zheng, Xuan"],["dc.contributor.author","Zhang, Lin"],["dc.contributor.author","Venkataramani, Vivek"],["dc.contributor.author","Jin, Fengyan"],["dc.contributor.author","Hein, Katharina"],["dc.contributor.author","Doeppner, Thorsten R."],["dc.date.accessioned","2021-06-01T09:41:26Z"],["dc.date.available","2021-06-01T09:41:26Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1016/j.neuropharm.2020.108357"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84920"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.issn","0028-3908"],["dc.title","Lithium enhances post-stroke blood-brain barrier integrity, activates the MAPK/ERK1/2 pathway and alters immune cell migration in mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Cellular Neuroscience"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Janssen, Lisa"],["dc.contributor.author","Ai, Xiaoyu"],["dc.contributor.author","Zheng, Xuan"],["dc.contributor.author","Wei, Wei"],["dc.contributor.author","Caglayan, Ahmet B."],["dc.contributor.author","Kilic, Ertugrul"],["dc.contributor.author","Wang, Ya-chao"],["dc.contributor.author","Hermann, Dirk M."],["dc.contributor.author","Venkataramani, Vivek"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Doeppner, Thorsten R."],["dc.date.accessioned","2021-10-01T09:58:18Z"],["dc.date.available","2021-10-01T09:58:18Z"],["dc.date.issued","2021"],["dc.description.abstract","Inhibition of fatty acid synthesis (FAS) stimulates tumor cell death and reduces angiogenesis. When SH-SY5Y cells or primary neurons are exposed to hypoxia only, inhibition of FAS yields significantly enhanced cell injury. The pathophysiology of stroke, however, is not only restricted to hypoxia but also includes reoxygenation injury. Hence, an oxygen-glucose-deprivation (OGD) model with subsequent reoxygenation in both SH-SY5Y cells and primary neurons as well as a murine stroke model were used herein in order to study the role of FAS inhibition and its underlying mechanisms. SH-SY5Y cells and cortical neurons exposed to 10 h of OGD and 24 h of reoxygenation displayed prominent cell death when treated with the Acetyl-CoA carboxylase inhibitor TOFA or the fatty acid synthase inhibitor cerulenin. Such FAS inhibition reduced the reduction potential of these cells, as indicated by increased NADH 2 + /NAD + ratios under both in vitro and in vivo stroke conditions. As observed in the OGD model, FAS inhibition also resulted in increased cell death in the stroke model. Stroke mice treated with cerulenin did not only display increased brain injury but also showed reduced neurological recovery during the observation period of 4 weeks. Interestingly, cerulenin treatment enhanced endothelial cell leakage, reduced transcellular electrical resistance (TER) of the endothelium and contributed to poststroke blood-brain barrier (BBB) breakdown. The latter was a consequence of the activated NF-κB pathway, stimulating MMP-9 and ABCB1 transporter activity on the luminal side of the endothelium. In conclusion, FAS inhibition aggravated poststroke brain injury as consequence of BBB breakdown and NF-κB-dependent inflammation."],["dc.description.abstract","Inhibition of fatty acid synthesis (FAS) stimulates tumor cell death and reduces angiogenesis. When SH-SY5Y cells or primary neurons are exposed to hypoxia only, inhibition of FAS yields significantly enhanced cell injury. The pathophysiology of stroke, however, is not only restricted to hypoxia but also includes reoxygenation injury. Hence, an oxygen-glucose-deprivation (OGD) model with subsequent reoxygenation in both SH-SY5Y cells and primary neurons as well as a murine stroke model were used herein in order to study the role of FAS inhibition and its underlying mechanisms. SH-SY5Y cells and cortical neurons exposed to 10 h of OGD and 24 h of reoxygenation displayed prominent cell death when treated with the Acetyl-CoA carboxylase inhibitor TOFA or the fatty acid synthase inhibitor cerulenin. Such FAS inhibition reduced the reduction potential of these cells, as indicated by increased NADH 2 + /NAD + ratios under both in vitro and in vivo stroke conditions. As observed in the OGD model, FAS inhibition also resulted in increased cell death in the stroke model. Stroke mice treated with cerulenin did not only display increased brain injury but also showed reduced neurological recovery during the observation period of 4 weeks. Interestingly, cerulenin treatment enhanced endothelial cell leakage, reduced transcellular electrical resistance (TER) of the endothelium and contributed to poststroke blood-brain barrier (BBB) breakdown. The latter was a consequence of the activated NF-κB pathway, stimulating MMP-9 and ABCB1 transporter activity on the luminal side of the endothelium. In conclusion, FAS inhibition aggravated poststroke brain injury as consequence of BBB breakdown and NF-κB-dependent inflammation."],["dc.identifier.doi","10.3389/fncel.2021.733973"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/90034"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-469"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1662-5102"],["dc.rights","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Inhibition of Fatty Acid Synthesis Aggravates Brain Injury, Reduces Blood-Brain Barrier Integrity and Impairs Neurological Recovery in a Murine Stroke Model"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Cellular Neuroscience"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Doeppner, Thorsten R."],["dc.contributor.author","Zechmeister, Bozena"],["dc.contributor.author","Kaltwasser, Britta"],["dc.contributor.author","Jin, Fengyan"],["dc.contributor.author","Zheng, Xuan"],["dc.contributor.author","Majid, Arshad"],["dc.contributor.author","Venkataramani, Vivek"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Hermann, Dirk M."],["dc.date.accessioned","2020-12-10T18:44:31Z"],["dc.date.available","2020-12-10T18:44:31Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.3389/fncel.2018.00383"],["dc.identifier.eissn","1662-5102"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78485"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Very Delayed Remote Ischemic Post-conditioning Induces Sustained Neurological Recovery by Mechanisms Involving Enhanced Angioneurogenesis and Peripheral Immunosuppression Reversal"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","357"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","STEM CELLS Translational Medicine"],["dc.bibliographiccitation.lastpage","373"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Haupt, Matteo"],["dc.contributor.author","Zheng, Xuan"],["dc.contributor.author","Kuang, Yaoyun"],["dc.contributor.author","Lieschke, Simone"],["dc.contributor.author","Janssen, Lisa"],["dc.contributor.author","Bosche, Bert"],["dc.contributor.author","Jin, Fengyan"],["dc.contributor.author","Hein, Katharina"],["dc.contributor.author","Kilic, Ertugrul"],["dc.contributor.author","Venkataramani, Vivek"],["dc.contributor.author","Hermann, Dirk M."],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Doeppner, Thorsten R."],["dc.date.accessioned","2021-04-14T08:32:17Z"],["dc.date.available","2021-04-14T08:32:17Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1002/sctm.20-0086"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83874"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","2157-6580"],["dc.relation.issn","2157-6564"],["dc.title","Lithium modulates miR ‐1906 levels of mesenchymal stem cell‐derived extracellular vesicles contributing to poststroke neuroprotection by toll‐like receptor 4 regulation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1127"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Arteriosclerosis, Thrombosis, and Vascular Biology"],["dc.bibliographiccitation.lastpage","1145"],["dc.bibliographiccitation.volume","41"],["dc.contributor.author","Zhang, Lin"],["dc.contributor.author","Graf, Irina"],["dc.contributor.author","Kuang, Yaoyun"],["dc.contributor.author","Zheng, Xuan"],["dc.contributor.author","Haupt, Matteo"],["dc.contributor.author","Majid, Arshad"],["dc.contributor.author","Kilic, Ertugrul"],["dc.contributor.author","Hermann, Dirk M."],["dc.contributor.author","Psychogios, Marios-Nikos"],["dc.contributor.author","Doeppner, Thorsten R."],["dc.date.accessioned","2021-06-01T09:42:10Z"],["dc.date.available","2021-06-01T09:42:10Z"],["dc.date.issued","2021"],["dc.description.abstract","Objective: Extracellular vesicles (EVs) derived from neural progenitor cells enhance poststroke neurological recovery, albeit the underlying mechanisms remain elusive. Since previous research described an enhanced poststroke integrity of the blood-brain barrier (BBB) upon systemic transplantation of neural progenitor cells, we examined if neural progenitor cell-derived EVs affect BBB integrity and which cellular mechanisms are involved in the process. Approach and Results: Using in vitro models of primary brain endothelial cell (EC) cultures as well as co-cultures of brain ECs (ECs) and astrocytes exposed to oxygen glucose deprivation, we examined the effects of EVs or vehicle on microvascular integrity. In vitro data were confirmed using a mouse transient middle cerebral artery occlusion model. Cultured ECs displayed increased ABCB1 (ATP-binding cassette transporter B1) levels when exposed to oxygen glucose deprivation, which was reversed by treatment with EVs. The latter was due to an EV-induced inhibition of the NF-κB (nuclear factor-κB) pathway. Using a BBB co-culture model of ECs and astrocytes exposed to oxygen glucose deprivation, EVs stabilized the BBB and ABCB1 levels without affecting the transcellular electrical resistance of ECs. Likewise, EVs yielded reduced Evans blue extravasation, decreased ABCB1 expression as well as an inhibition of the NF-κB pathway, and downstream matrix metalloproteinase 9 (MMP-9) activity in stroke mice. The EV-induced inhibition of the NF-κB pathway resulted in a poststroke modulation of immune responses. Conclusions: Our findings suggest that EVs enhance poststroke BBB integrity via ABCB1 and MMP-9 regulation, attenuating inflammatory cell recruitment by inhibition of the NF-κB pathway. Graphic Abstract: A graphic abstract is available for this article."],["dc.identifier.doi","10.1161/ATVBAHA.120.315031"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85166"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1524-4636"],["dc.relation.issn","1079-5642"],["dc.title","Neural Progenitor Cell-Derived Extracellular Vesicles Enhance Blood-Brain Barrier Integrity by NF-κB (Nuclear Factor-κB)-Dependent Regulation of ABCB1 (ATP-Binding Cassette Transporter B1) in Stroke Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Extracellular Vesicles"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Kuang, Yaoyun"],["dc.contributor.author","Zheng, Xuan"],["dc.contributor.author","Zhang, Lin"],["dc.contributor.author","Ai, Xiaoyu"],["dc.contributor.author","Venkataramani, Vivek"],["dc.contributor.author","Kilic, Ertugrul"],["dc.contributor.author","Hermann, Dirk M."],["dc.contributor.author","Majid, Arshad"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Doeppner, Thorsten R."],["dc.date.accessioned","2021-04-14T08:32:18Z"],["dc.date.available","2021-04-14T08:32:18Z"],["dc.date.issued","2020"],["dc.description.sponsorship","Open-Access-Finanzierung durch die Universitätsmedizin Göttingen 2021"],["dc.identifier.doi","10.1002/jev2.12024"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17797"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83879"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.notes.intern","In goescholar not merged with http://resolver.sub.uni-goettingen.de/purl?gs-1/17840 but duplicate"],["dc.relation.eissn","2001-3078"],["dc.relation.issn","2001-3078"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Adipose‐derived mesenchymal stem cells reduce autophagy in stroke mice by extracellular vesicle transfer of miR‐25"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","66"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Cells"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Lieschke, Simone"],["dc.contributor.author","Zechmeister, Bozena"],["dc.contributor.author","Haupt, Matteo"],["dc.contributor.author","Zheng, Xuan"],["dc.contributor.author","Jin, Fengyan"],["dc.contributor.author","Hein, Katharina"],["dc.contributor.author","Weber, Martin S."],["dc.contributor.author","Hermann, Dirk M."],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Kilic, Ertugrul"],["dc.contributor.author","Doeppner, Thorsten R."],["dc.date.accessioned","2020-12-10T18:46:59Z"],["dc.date.available","2020-12-10T18:46:59Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.3390/cells9010066"],["dc.identifier.eissn","2073-4409"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17054"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78606"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","MDPI"],["dc.relation.eissn","2073-4409"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","CCL11 Differentially Affects Post-Stroke Brain Injury and Neuroregeneration in Mice Depending on Age"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5995"],["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","20"],["dc.contributor.affiliation","Zheng, Xuan; \t\t \r\n\t\t Department of Neurology, University of Goettingen Medical School, 37075 Goettingen, Germany, xuan.zheng.1988@gmail.com"],["dc.contributor.affiliation","Bähr, Mathias; \t\t \r\n\t\t Department of Neurology, University of Goettingen Medical School, 37075 Goettingen, Germany, mbaehr@gwdg.de"],["dc.contributor.affiliation","Doeppner, Thorsten R.; \t\t \r\n\t\t Department of Neurology, University of Goettingen Medical School, 37075 Goettingen, Germany, thorsten.doeppner@med.uni-goettingen.de"],["dc.contributor.author","Zheng, Xuan"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Doeppner, Thorsten R."],["dc.date.accessioned","2020-12-10T18:47:09Z"],["dc.date.available","2020-12-10T18:47:09Z"],["dc.date.issued","2019"],["dc.date.updated","2022-09-07T05:31:52Z"],["dc.identifier.doi","10.3390/ijms20235995"],["dc.identifier.eissn","1422-0067"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17108"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78662"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","From Tumor Metastasis towards Cerebral Ischemia—Extracellular Vesicles as a General Concept of Intercellular Communication Processes"],["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","403"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Stem Cells"],["dc.bibliographiccitation.lastpage","413"],["dc.bibliographiccitation.volume","39"],["dc.contributor.author","Zheng, Xuan"],["dc.contributor.author","Hermann, Dirk M."],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Doeppner, Thorsten R."],["dc.date.accessioned","2021-04-22T14:35:05Z"],["dc.date.available","2021-04-22T14:35:05Z"],["dc.date.issued","2021"],["dc.description.abstract","The heart and the brain mutually interact with each other, forming a functional axis that is disturbed under conditions of ischemia. Stem cell-derived extracellular vesicles (EVs) show great potential for the treatment of ischemic stroke and myocardial infarction. Due to heart-brain interactions, therapeutic actions of EVs in the brain and the heart cannot be regarded in an isolated way. Effects in each of the two organs reciprocally influence the outcome of the other. Stem cell-derived EVs modulate a large number of signaling pathways in both tissues. Upon ischemia, EVs prevent delayed injury, promote angiogenesis, enhance parenchymal remodeling, and enable functional tissue recovery. The therapeutic effects greatly depend on EV cargos, among which are noncoding RNAs like microRNAs (miRNAs) and proteins, which modulate cell signaling in a differential way that not always corresponds to each other in the two tissues. Interestingly, the same miRNA or protein localized in EVs can modulate different signaling pathways in the ischemic heart and brain, which may have diverse consequences for disease outcomes. Paying careful attention to unveiling these underlying mechanisms may provide new insights into tissue remodeling processes and identify targets for ischemic stroke and myocardial infarction therapies. Some of these mechanisms are discussed in this concise review, and consequences for the clinical translation of EVs are presented."],["dc.identifier.doi","10.1002/stem.3329"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84318"],["dc.language.iso","en"],["dc.notes.intern","DeepGreen Import"],["dc.publisher","John Wiley & Sons, Inc."],["dc.rights","This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes."],["dc.title","The role of small extracellular vesicles in cerebral and myocardial ischemia-Molecular signals, treatment targets, and future clinical translation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]