Döppner, Thorsten Roland

[["dc.bibliographiccitation.firstpage","1297"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","STEM CELLS"],["dc.bibliographiccitation.lastpage","1310"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Doeppner, T. R."],["dc.contributor.author","Ewert, T. A. S."],["dc.contributor.author","Tönges, L."],["dc.contributor.author","Herz, J."],["dc.contributor.author","Zechariah, A."],["dc.contributor.author","Elali, A."],["dc.contributor.author","Ludwig, A.-K."],["dc.contributor.author","Giebel, B."],["dc.contributor.author","Nagel, F."],["dc.contributor.author","Dietz, G. P. H."],["dc.contributor.author","Weise, J."],["dc.contributor.author","Hermann, D. M."],["dc.contributor.author","Bähr, M."],["dc.date.accessioned","2017-09-07T11:48:52Z"],["dc.date.available","2017-09-07T11:48:52Z"],["dc.date.issued","2012"],["dc.description.abstract","Novel therapeutic concepts against cerebral ischemia focus on cell-based therapies in order to overcome some of the side effects of thrombolytic therapy. However, cell-based therapies are hampered because of restricted understanding regarding optimal cell transplantation routes and due to low survival rates of grafted cells. We therefore transplanted adult green fluorescence protein positive neural precursor cells (NPCs) either intravenously (systemic) or intrastriatally (intracerebrally) 6 hours after stroke in mice. To enhance survival of NPCs, cells were in vitro protein-transduced with TAT-heat shock protein 70 (Hsp70) before transplantation followed by a systematic analysis of brain injury and underlying mechanisms depending on cell delivery routes. Transduction of NPCs with TAT-Hsp70 resulted in increased intracerebral numbers of grafted NPCs after intracerebral but not after systemic transplantation. Whereas systemic delivery of either native or transduced NPCs yielded sustained neuroprotection and induced neurological recovery, only TAT-Hsp70-transduced NPCs prevented secondary neuronal degeneration after intracerebral delivery that was associated with enhanced functional outcome. Furthermore, intracerebral transplantation of TAT-Hsp70-transduced NPCs enhanced postischemic neurogenesis and induced sustained high levels of brain-derived neurotrophic factor, glial cell line-derived neurotrophic factor, and vascular endothelial growth factor in vivo. Neuroprotection after intracerebral cell delivery correlated with the amount of surviving NPCs. On the contrary, systemic delivery of NPCs mediated acute neuroprotection via stabilization of the blood-brain-barrier, concomitant with reduced activation of matrix metalloprotease 9 and decreased formation of reactive oxygen species. Our findings imply two different mechanisms of action of intracerebrally and systemically transplanted NPCs, indicating that systemic NPC delivery might be more feasible for translational stroke concepts, lacking a need of in vitro manipulation of NPCs to induce long-term neuroprotection. STEM CELLS2012;30:12971310"],["dc.identifier.doi","10.1002/stem.1098"],["dc.identifier.gro","3142531"],["dc.identifier.isi","000304087300026"],["dc.identifier.pmid","22593021"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8892"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1066-5099"],["dc.title","Transduction of Neural Precursor Cells with TAT-Heat Shock Protein 70 Chaperone: Therapeutic Potential Against Ischemic Stroke after Intrastriatal and Systemic Transplantation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["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.artnumber","oeab022"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","European Heart Journal Open"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","Jin, Fengyan"],["dc.contributor.author","Li, Jian"],["dc.contributor.author","Guo, Jianfeng"],["dc.contributor.author","Doeppner, Thorsten R."],["dc.contributor.author","Hermann, Dirk M"],["dc.contributor.author","Yao, Gang"],["dc.contributor.author","Dai, Yun"],["dc.date.accessioned","2022-09-01T09:50:28Z"],["dc.date.available","2022-09-01T09:50:28Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract\r\n Epigenomic and epigenetic research has been providing several new insights into a variety of diseases caused by non-resolving inflammation, including cardiovascular diseases. Atherosclerosis (AS) has long been recognized as a chronic inflammatory disease of the arterial walls, characterized by local persistent and stepwise accelerating inflammation without resolution, also known as uncontrolled inflammation. The pathogenesis of AS is driven primarily by highly plastic macrophages via their polarization to pro- or anti-inflammatory phenotypes as well as other novel subtypes recently identified by single-cell sequencing. Although emerging evidence has indicated the key role of the epigenetic machinery in the regulation of macrophage plasticity, the investigation of epigenetic alterations and modifiers in AS and related inflammation is still in its infancy. An increasing number of the epigenetic modifiers (e.g. TET2, DNMT3A, HDAC3, HDAC9, JMJD3, KDM4A) have been identified in epigenetic remodelling of macrophages through DNA methylation or histone modifications (e.g. methylation, acetylation, and recently lactylation) in inflammation. These or many unexplored modifiers function to determine or switch the direction of macrophage polarization via transcriptional reprogramming of gene expression and intracellular metabolic rewiring upon microenvironmental cues, thereby representing a promising target for anti-inflammatory therapy in AS. Here, we review up-to-date findings involving the epigenetic regulation of macrophages to shed light on the mechanism of uncontrolled inflammation during AS onset and progression. We also discuss current challenges for developing an effective and safe anti-AS therapy that targets the epigenetic modifiers and propose a potential anti-inflammatory strategy that repolarizes macrophages from pro- to anti-inflammatory phenotypes."],["dc.identifier.doi","10.1093/ehjopen/oeab022"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/113721"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-597"],["dc.relation.eissn","2752-4191"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.relation.orgunit","Klinik für Neurologie"],["dc.rights","CC BY-NC 4.0"],["dc.title","Targeting epigenetic modifiers to reprogramme macrophages in non-resolving inflammation-driven atherosclerosis"],["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","4902"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Current Issues in Molecular Biology"],["dc.bibliographiccitation.lastpage","4920"],["dc.bibliographiccitation.volume","44"],["dc.contributor.author","Coliță, Daniela"],["dc.contributor.author","Coliță, Cezar-Ivan"],["dc.contributor.author","Hermann, Dirk"],["dc.contributor.author","Coliță, Eugen"],["dc.contributor.author","Doeppner, Thorsten"],["dc.contributor.author","Udristoiu, Ion"],["dc.contributor.author","Popa-Wagner, Aurel"],["dc.date.accessioned","2022-12-01T08:31:38Z"],["dc.date.available","2022-12-01T08:31:38Z"],["dc.date.issued","2022"],["dc.description.abstract","The available evidence suggests that affective disorders, such as depression and anxiety, increase risk for accelerated cognitive decline and late-life dementia in aging individuals. Behavioral neuropsychology studies also showed that cognitive decline is a central feature of aging impacting the quality of life. Motor deficits are common after traumatic brain injuries and stroke, affect subjective well-being, and are linked with reduced quality of life. Currently, restorative therapies that target the brain directly to restore cognitive and motor tasks in aging and disease are available. However, the very same drugs used for therapeutic purposes are employed by athletes as stimulants either to increase performance for fame and financial rewards or as recreational drugs. Unfortunately, most of these drugs have severe side effects and pose a serious threat to the health of athletes. The use of performance-enhancing drugs by children and teenagers has increased tremendously due to the decrease in the age of players in competitive sports and the availability of various stimulants in many forms and shapes. Thus, doping may cause serious health-threatening conditions including, infertility, subdural hematomas, liver and kidney dysfunction, peripheral edema, cardiac hypertrophy, myocardial ischemia, thrombosis, and cardiovascular disease. In this review, we focus on the impact of doping on psychopathological disorders, cognition, and depression. Occasionally, we also refer to chronic use of therapeutic drugs to increase physical performance and highlight the underlying mechanisms. We conclude that raising awareness on the health risks of doping in sport for all shall promote an increased awareness for healthy lifestyles across all generations."],["dc.identifier.doi","10.3390/cimb44100333"],["dc.identifier.pii","cimb44100333"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118225"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-621"],["dc.relation.eissn","1467-3045"],["dc.title","Therapeutic Use and Chronic Abuse of CNS Stimulants and Anabolic Drugs"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","57"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Restorative neurology and neuroscience"],["dc.bibliographiccitation.lastpage","64"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Weise, Jens"],["dc.contributor.author","Doeppner, Thorsten R."],["dc.contributor.author","Müller, T."],["dc.contributor.author","Wrede, Arne"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Witte, Otto W."],["dc.contributor.author","Bähr, M."],["dc.date.accessioned","2017-09-07T11:48:49Z"],["dc.date.available","2017-09-07T11:48:49Z"],["dc.date.issued","2008"],["dc.description.abstract","Purpose: The physiological function of the cellular prion protein (PrP(C)) is still unclear. A growing body of evidence suggests that PrP(C) has neuroprotective properties and that its deletion increases susceptibility to focal cerebral ischemia. The purpose of this study was to elucidate the role of PrP(C) overexpression in ischemic brain injury in vivo. Methods: PrP(C) overexpressing (TG35) and wild type (WT) mice were subjected to a 90-minute transient focal cerebral ischemia followed by infarct volume analysis 24 hours after lesion. To identify effects of PrP(C) overexpression on signalling pathways important for the regulation of ischemic cell death, we studied postischemic activation and expression of Akt and Erk1/2 using quantitative Western Blot analysis. Results: TG35 mice displayed significantly smaller infarct volumes and showed reduced early postischemic Erk1/2 phosphorylation, a pathway known to exacerbate neuronal injury following transient cerebral ischemia. In contrast, PrP(C) overexpression did not change postischemic Akt phosphorylation, which acts anti-apoptotic and is reduced in PrP(C) knockout animals. Conclusions: These results demonstrate that PrP(C) overexpression reduces deleterious Erk1/2 activation but does not affect Akt activation after transient cerebral ischemia, suggesting a role for distinct cytosolic signalling pathways in PrP(C) mediated neuroprotection."],["dc.identifier.gro","3143388"],["dc.identifier.isi","000256236700005"],["dc.identifier.pmid","18431006"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/896"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0922-6028"],["dc.title","Overexpression of cellular prion protein alters postischemic Erk1/2 phosphorylation but not Akt phosphorylation and protects against focal cerebral ischemia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]