Döppner, Thorsten Roland

[["dc.bibliographiccitation.firstpage","429"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","442"],["dc.bibliographiccitation.volume","122"],["dc.contributor.author","Doeppner, T. R."],["dc.contributor.author","Bretschneider, E."],["dc.contributor.author","Doehring, M."],["dc.contributor.author","Segura, I."],["dc.contributor.author","Sentürk, A."],["dc.contributor.author","Acker-Palmer, A."],["dc.contributor.author","Hasan, M. R."],["dc.contributor.author","Elali, A."],["dc.contributor.author","Hermann, D. M."],["dc.contributor.author","Bähr, M."],["dc.date.accessioned","2017-09-07T11:43:22Z"],["dc.date.available","2017-09-07T11:43:22Z"],["dc.date.issued","2011"],["dc.description.abstract","Cerebral ischemia stimulates endogenous neurogenesis. However, the functional relevance of this phenomenon remains unclear because of poor survival and low neuronal differentiation rates of newborn cells. Therefore, further studies on mechanisms regulating neurogenesis under ischemic conditions are required, among which ephrin-ligands and ephrin-receptors (Eph) are an interesting target. Although Eph/ephrin proteins like ephrin-B3 are known to negatively regulate neurogenesis under physiological conditions, their role in cerebral ischemia is largely unknown. We therefore studied neurogenesis, brain injury and functional outcome in ephrin-B3(-/-) (knockout) and ephrin-B3(+/+) (wild-type) mice submitted to cerebral ischemia. Induction of stroke resulted in enhanced cell proliferation and neuronal differentiation around the lesion site of ephrin-B3(-/-) compared to ephrin-B3(+/+) mice. However, prominent post-ischemic neurogenesis in ephrin-B3(-/-) mice was accompanied by significantly increased ischemic injury and motor coordination deficits that persisted up to 4 weeks. Ischemic injury in ephrin-B3(-/-) mice was associated with a caspase-3-dependent activation of the signal transducer and activator of transcription 1 (STAT1). Whereas inhibition of caspase-3 had no effect on brain injury in ephrin-B3(+/+) animals, infarct size in ephrin-B3(-/-) mice was strongly reduced, suggesting that aggravated brain injury in these animals might involve a caspase-3-dependent activation of STAT1. In conclusion, post-ischemic neurogenesis in ephrin-B3(-/-) mice is strongly enhanced, but fails to contribute to functional recovery because of caspase-3-mediated aggravation of ischemic injury in these animals. Our results suggest that ephrin-B3 might be an interesting target for overcoming some of the limitations of further cell-based therapies in stroke."],["dc.identifier.doi","10.1007/s00401-011-0856-5"],["dc.identifier.gro","3142655"],["dc.identifier.isi","000296506000004"],["dc.identifier.pmid","21779764"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7316"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0001-6322"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject","Caspase-3; Cerebral ischemia; Endogenous neurogenesis; Ephrin-B3; Neural precursor cells; STAT1"],["dc.title","Enhancement of endogenous neurogenesis in ephrin-B3 deficient mice after transient focal cerebral ischemia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["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.artnumber","e2024"],["dc.bibliographiccitation.journal","Cell Death and Disease"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Doeppner, T. R."],["dc.contributor.author","Kaltwasser, B."],["dc.contributor.author","Schlechter, J."],["dc.contributor.author","Jaschke, J."],["dc.contributor.author","Kilic, E."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Hermann, D. M."],["dc.contributor.author","Weise, J."],["dc.date.accessioned","2017-09-07T11:54:49Z"],["dc.date.available","2017-09-07T11:54:49Z"],["dc.date.issued","2015"],["dc.description.abstract","Although cellular prion protein (PrPc) has been suggested to have physiological roles in neurogenesis and angiogenesis, the pathophysiological relevance of both processes remain unknown. To elucidate the role of PrPc in post-ischemic brain remodeling, we herein exposed PrPc wild type (WT), PrPc knockout (PrP -/-) and PrPc overexpressing (PrP+/+) mice to focal cerebral ischemia followed by up to 28 days reperfusion. Improved neurological recovery and sustained neuroprotection lasting over the observation period of 4 weeks were observed in ischemic PrP+/+ mice compared with WT mice. This observation was associated with increased neurogenesis and angiogenesis, whereas increased neurological deficits and brain injury were noted in ischemic PrP-/- mice. Proteasome activity and oxidative stress were increased in ischemic brain tissue of PrP -/- mice. Pharmacological proteasome inhibition reversed the exacerbation of brain injury induced by PrP -/-, indicating that proteasome inhibition mediates the neuroprotective effects of PrPc. Notably, reduced proteasome activity and oxidative stress in ischemic brain tissue of PrP+/+ mice were associated with an increased abundance of hypoxia-inducible factor 1 alpha and PACAP-38, which are known stimulants of neural progenitor cell (NPC) migration and trafficking. To elucidate effects of PrPc on intracerebral NPC homing, we intravenously infused GFP(+) NPCs in ischemic WT, PrP -/- and PrP+/+ mice, showing that brain accumulation of GFP+ NPCs was greatly reduced in PrP -/- mice, but increased in PrP+/+ animals. Our results suggest that PrPc induces post-ischemic long-term neuroprotection, neurogenesis and angiogenesis in the ischemic brain by inhibiting proteasome activity."],["dc.identifier.doi","10.1038/cddis.2015.365"],["dc.identifier.gro","3141770"],["dc.identifier.isi","000368172400023"],["dc.identifier.pmid","26673668"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12863"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/879"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: TUBITAK [2221]; German Research Council [HE3173/2-2, HE3173/3-1]"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","2041-4889"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject","Cell signalling; Ischaemia; Proteasome; Stroke"],["dc.title","Cellular prion protein promotes post-ischemic neuronal survival, angioneurogenesis and enhances neural progenitor cell homing via proteasome inhibition"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["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.firstpage","570"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Translational Oncology"],["dc.bibliographiccitation.lastpage","579"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Mlynarczuk-Bialy, Izabela"],["dc.contributor.author","Doeppner, Thorsten R."],["dc.contributor.author","Golab, Jakub"],["dc.contributor.author","Nowis, Dominika"],["dc.contributor.author","Wilczynski, Grzegorz M."],["dc.contributor.author","Parobczak, Kamil"],["dc.contributor.author","Wigand, Moritz E."],["dc.contributor.author","Hajdamowicz, Malgorzata"],["dc.contributor.author","Bialy, Lukasz P."],["dc.contributor.author","Aniolek, Olga"],["dc.contributor.author","Henklein, Petra"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Schmidt, Boris"],["dc.contributor.author","Kuckelkorn, Ulrike"],["dc.contributor.author","Kloetzel, Peter-M."],["dc.date.accessioned","2017-09-07T11:45:27Z"],["dc.date.available","2017-09-07T11:45:27Z"],["dc.date.issued","2014"],["dc.description.abstract","Inhibition of the proteasome offers many therapeutic possibilities in inflammation as well as in neoplastic diseases. However, clinical use of proteasome inhibitors is limited by the development of resistance or severe side effects. In our study we characterized the anti-tumor properties of the novel proteasome inhibitor BSc2118. The sensitivity of tumor lines to BSc2118 was analyzed in comparison to bortezomib using crystal violet staining in order to assess cell viability. The In Vivo distribution of BSc2118 in mouse tissues was tracked by a fluorescent-modified form of BSc2118 (BSc2118-FL) and visualized by confocal microscopy. Inhibition of the 20S proteasome was monitored both in cultured cell lines and in mice, respectively. Finally, safety and efficacy of BSc2118 was evaluated in a mouse melanoma model. BSc2118 inhibits proliferation of different tumor cell lines with a similar potency as compared with bortezomib. Systemic administration of BSc2118 in mice is well tolerated, even when given in a dose of 60 mg/kg body weight. After systemic injection of BSc2118 or bortezomib similar proteasome inhibition patterns are observed within the murine organs. Detection of BSc2118-FL revealed correlation of distribution pattern of BSc2118 with inhibition of proteasomal activity in cells or mouse tissues. Finally, administration of BSc2118 in a mouse melanoma model shows significant local anti-tumor effects. Concluding, BSc2118 represents a novel low-toxic agent that might be alternatively used for known proteasome inhibitors in anti-cancer treatment."],["dc.identifier.doi","10.1016/j.tranon.2014.07.002"],["dc.identifier.gro","3142039"],["dc.identifier.isi","000348837100005"],["dc.identifier.pmid","25389452"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11362"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/3867"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Polish Ministry of Science and higher Education [N405 007 31/0544]"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1936-5233"],["dc.relation.issn","1944-7124"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","Biodistribution and Efficacy Studies of the Proteasome Inhibitor BSc2118 in a Mouse Melanoma Model"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","593"],["dc.bibliographiccitation.journal","Frontiers in Physiology"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Bosche, Bert"],["dc.contributor.author","Moicanyi, Marek"],["dc.contributor.author","Rej, Soham"],["dc.contributor.author","Doeppner, Thorsten R."],["dc.contributor.author","Obermann, Mark"],["dc.contributor.author","Das, Anupam"],["dc.contributor.author","Macdonald, R. Loch"],["dc.contributor.author","Noll, Thomas"],["dc.contributor.author","Müller, Daniel J."],["dc.contributor.author","Hescheler, Jürgen"],["dc.contributor.author","Härtel, Frauke V."],["dc.date.accessioned","2018-11-07T10:04:37Z"],["dc.date.available","2018-11-07T10:04:37Z"],["dc.date.issued","2016"],["dc.description.abstract","Lithium at serum concentrations up to 1 mmol/L has been used in patients suffering from bipolar disorder for decades and has recently been shown to reduce the risk for ischemic stroke in these patients. The risk for stroke and thromboembolism depend not only on cerebral but also on general endothelial function and health; the entire endothelium as an organ is therefore pathophysiologically relevant. Regardless, the knowledge about the direct impact of lithium on endothelial function remains poor. We conducted an experimental study using lithium as pharmacologic pretreatment for murine, porcine and human vascular endothelium. We predominantly investigated endothelial vasorelaxation capacities in addition to human basal and dynamic (thrombin-/PAR-1 receptor agonist-impaired) barrier functioning including myosin light chain (MLC) phosphorylation (MLC-P). Low-dose therapeutic lithium concentrations (0.4 mmol/L) significantly augment the cholinergic endothelium-dependent vasorelaxation capacities of cerebral and thoracic arteries, independently of central and autonomic nerve system influences. Similar concentrations of lithium (0.2-0.4 mmol/L) significantly stabilized the dynamic thrombin -induced and PAR-1 receptor agonist-induced permeability of human endothelium, while even the basal permeability appeared to be stabilized. The lithium attenuated dynamic permeability was mediated by a reduced endothelial MLC-P known to be followed by a lessening of endothelial cell contraction and paracellular gap formation. The well-known lithium-associated inhibition of inositol monophosphatase/glycogen synthase kinase-3-beta signaling-pathways involving intracellular calcium concentrations in neurons seems to similarly occur in endothelial cells, too, but with different down-stream effects such as MLC-P reduction. This is the first study discovering low dose lithium as a drug directly stabilizing human endothelium and ubiquitously augmenting cholinergic endothelium-mediated vasorelaxation. Our findings have translational and potentially clinical impact on cardiovascular and cerebrovascular disease associated with inflammation explaining why lithium can reduce, e.g., the risk for stroke. However, further clinical studies are warranted."],["dc.identifier.doi","10.3389/fphys.2016.00593"],["dc.identifier.isi","000389378100001"],["dc.identifier.pmid","27999548"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14072"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38735"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1664-042X"],["dc.relation.issn","1664-042X"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Low-Dose Lithium Stabilizes Human Endothelial Barrier by Decreasing MLC Phosphorylation and Universally Augments Cholinergic Vasorelaxation Capacity in a Direct Manner"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","338"],["dc.bibliographiccitation.journal","Frontiers in Cellular Neuroscience"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Doeppner, Thorsten R."],["dc.contributor.author","Kaltwasser, Britta"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Hermann, Dirk M."],["dc.date.accessioned","2017-09-07T11:45:26Z"],["dc.date.available","2017-09-07T11:45:26Z"],["dc.date.issued","2014"],["dc.description.abstract","Systemic transplantation of neural progenitor cells (NPCs) in rodents reduces functional impairment after cerebral ischemia. In light of upcoming stroke trials regarding safety and feasibility of NPC transplantation, experimental studies have to successfully analyze the extent of NPC-induced neurorestoration on the functional level. However, appropriate behavioral tests for analysis of post-stroke motor coordination deficits and cognitive impairment after NPC grafting are not fully established. We therefore exposed male C57BL6 mice to either 45 min (mild) or 90 min (severe) of cerebral ischemia, using the thread occlusion model followed by intravenous injection of PBS or NPCs 6 h post-stroke with an observation period of three months. Post-stroke motor coordination was assessed by means of the rota rod, tight rope, corner turn, inclined plane, grip strength, foot fault, adhesive removal, pole test and balance beam test, whereas cognitive impairment was analyzed using the water maze, the open field and the passive avoidance test. Significant motor coordination differences after both mild and severe cerebral ischemia in favor of NPC-treated mice were observed for each motor coordination test except for the inclined plane and the grip strength test, which only showed significant differences after severe cerebral ischemia. Cognitive impairment after mild cerebral ischemia was successfully assessed using the water maze test, the open field and the passive avoidance test. On the contrary, the water maze test was not suitable in the severe cerebral ischemia paradigm, as it too much depends on motor coordination capabilities of test mice. In terms of both reliability and cost-effectiveness considerations, we thus recommend the corner turn, foot fault, balance beam, and open field test, which do not depend on durations of cerebral ischemia."],["dc.identifier.doi","10.3389/fncel.2014.00338"],["dc.identifier.gro","3142031"],["dc.identifier.isi","000344535600001"],["dc.identifier.pmid","25374509"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11787"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/3778"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Deutsche Forschungsgemeinschaft [HE3173/2-1, HE3173/2-2, HE3173/3-1]"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1662-5102"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Effects of neural progenitor cells on post-stroke neurological impairment-a detailed and comprehensive analysis of behavioral tests"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3053"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","21"],["dc.contributor.affiliation","Jain, Saurabh; \t\t \r\n\t\t Department of Neuroscience, SITraN, University of Sheffield, Sheffield S10 2HQ, UK, s.a.jain@sheffield.ac.uk"],["dc.contributor.affiliation","Kim, Eun-Sun; \t\t \r\n\t\t College of Pharmacy, Institute of Pharmaceutical Science and Technology, Hanyang University, Ansan 15588, Korea, ikhhycs@hanmail.net"],["dc.contributor.affiliation","Kim, Donghyun; \t\t \r\n\t\t College of Pharmacy, Institute of Pharmaceutical Science and Technology, Hanyang University, Ansan 15588, Korea, ssks7787@naver.com"],["dc.contributor.affiliation","Burrows, David; \t\t \r\n\t\t Department of Neuroscience, SITraN, University of Sheffield, Sheffield S10 2HQ, UK, djburrows1@sheffield.ac.uk"],["dc.contributor.affiliation","De Felice, Milena; \t\t \r\n\t\t Department of Neuroscience, SITraN, University of Sheffield, Sheffield S10 2HQ, UK, m.defelice@sheffield.ac.uk"],["dc.contributor.affiliation","Kim, Minyeong; \t\t \r\n\t\t College of Pharmacy and Research, Institute of Pharmaceutical Science and Technology (RIPST), Ajou University, Suwon 16499, Korea, my1123@ajou.ac.kr"],["dc.contributor.affiliation","Baek, Seung-Hoon; \t\t \r\n\t\t College of Pharmacy and Research, Institute of Pharmaceutical Science and Technology (RIPST), Ajou University, Suwon 16499, Korea, shbaek@ajou.ac.kr"],["dc.contributor.affiliation","Ali, Ali; \t\t \r\n\t\t Department of Neuroscience, SITraN, University of Sheffield, Sheffield S10 2HQ, UK, Ali.Ali@sth.nhs.uk"],["dc.contributor.affiliation","Redgrave, Jessica; \t\t \r\n\t\t Department of Neuroscience, SITraN, University of Sheffield, Sheffield S10 2HQ, UK, Jessica.Redgrave@sth.nhs.uk"],["dc.contributor.affiliation","Doeppner, Thorsten R.; \t\t \r\n\t\t Department of Neurology, University Medical Center Goettingen, 37075 Goettingen, Germany, thorsten.doeppner@med.uni-goettingen.de"],["dc.contributor.affiliation","Gardner, Iain; \t\t \r\n\t\t Translation DMPK Sciences, Simcyp Division, Certara, Sheffield S1 2BJ, UK, iain.gardner@certara.com"],["dc.contributor.affiliation","Bae, Ok-Nam; \t\t \r\n\t\t College of Pharmacy, Institute of Pharmaceutical Science and Technology, Hanyang University, Ansan 15588, Korea, onbae@hanyang.ac.kr"],["dc.contributor.affiliation","Majid, Arshad; \t\t \r\n\t\t Department of Neuroscience, SITraN, University of Sheffield, Sheffield S10 2HQ, UK, arshad.majid@sheffield.ac.uk"],["dc.contributor.author","Jain, Saurabh"],["dc.contributor.author","Kim, Eun-Sun"],["dc.contributor.author","Kim, Donghyun"],["dc.contributor.author","Burrows, David"],["dc.contributor.author","De Felice, Milena"],["dc.contributor.author","Kim, Minyeong"],["dc.contributor.author","Baek, Seung-Hoon"],["dc.contributor.author","Ali, Ali"],["dc.contributor.author","Redgrave, Jessica"],["dc.contributor.author","Doeppner, Thorsten R."],["dc.contributor.author","Gardner, Iain"],["dc.contributor.author","Bae, Ok-Nam"],["dc.contributor.author","Majid, Arshad"],["dc.date.accessioned","2021-04-14T08:26:24Z"],["dc.date.available","2021-04-14T08:26:24Z"],["dc.date.issued","2020"],["dc.date.updated","2022-09-07T00:24:27Z"],["dc.description.sponsorship","National Research Foundation of Korea"],["dc.description.sponsorship","Medical Research Council"],["dc.identifier.doi","10.3390/ijms21093053"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81928"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Comparative Cerebroprotective Potential of d- and l-Carnosine Following Ischemic Stroke in Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e1386"],["dc.bibliographiccitation.journal","Cell Death and Disease"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Doeppner, Thorsten R."],["dc.contributor.author","Kaltwasser, Britta"],["dc.contributor.author","Teli, M. K."],["dc.contributor.author","Bretschneider, Eva"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Hermann, Dirk M."],["dc.date.accessioned","2017-09-07T11:45:39Z"],["dc.date.available","2017-09-07T11:45:39Z"],["dc.date.issued","2014"],["dc.description.abstract","Intravenous transplantation of neural progenitor cells (NPCs) induces functional recovery after stroke, albeit grafted cells are not integrated into residing neural networks. However, a systematic analysis of intravenous NPC delivery at acute and post-acute time points and their long-term consequences does not exist. Male C57BL6 mice were exposed to cerebral ischemia, and NPCs were intravenously grafted on day 0, on day 1 or on day 28. Animals were allowed to survive for up to 84 days. Mice and tissues were used for immunohistochemical analysis, flow cytometry, ELISA and behavioral tests. Density of grafted NPCs within the ischemic hemisphere was increased when cells were transplanted on day 28 as compared with transplantation on days 0 or 1. Likewise, transplantation on day 28 yielded enhanced neuronal differentiation rates of grafted cells. Post-ischemic brain injury, however, was only reduced when NPCs were grafted at acute time points. On the contrary, reduced post-ischemic functional deficits due to NPC delivery were independent of transplantation paradigms. NPC-induced neuroprotection after acute cell delivery was due to stabilization of the blood-brain barrier (BBB), reduction in microglial activation and modulation of both peripheral and central immune responses. On the other hand, post-acute NPC transplantation stimulated post-ischemic regeneration via enhanced angioneurogenesis and increased axonal plasticity. Acute NPC delivery yields long-term neuroprotection via enhanced BBB integrity and modulation of post-ischemic immune responses, whereas post-acute NPC delivery increases post-ischemic angioneurogenesis and axonal plasticity. Post-ischemic functional recovery, however, is independent of NPC delivery timing, which offers a broad therapeutic time window for stroke treatment."],["dc.identifier.doi","10.1038/cddis.2014.359"],["dc.identifier.gro","3142080"],["dc.identifier.isi","000341639000027"],["dc.identifier.pmid","25144721"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12114"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/4322"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","2041-4889"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","Effects of acute versus post-acute systemic delivery of neural progenitor cells on neurological recovery and brain remodeling after focal cerebral ischemia in mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","14033"],["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","14044"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Jaeger, H. M."],["dc.contributor.author","Pehlke, J. R."],["dc.contributor.author","Kaltwasser, B."],["dc.contributor.author","Kilic, E."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Hermann, D. M."],["dc.contributor.author","Doeppner, T. R."],["dc.date.accessioned","2017-09-07T11:43:46Z"],["dc.date.available","2017-09-07T11:43:46Z"],["dc.date.issued","2015"],["dc.description.abstract","N-methyl-D-aspartate receptor (NMDAR) activation induces excitotoxicity, contributing to post-stroke brain injury. Hitherto, NMDAR deactivation failed in clinical trials due to insufficient pre-clinical study designs and drug toxicity. Flupirtine is an indirect NMDAR antagonist being used as analgesic in patients. Taking into account its tolerability profile, we evaluated effects of flupirtine on post-stroke tissue survival, neurological recovery and brain remodeling. Mice were exposed to stroke and intraperitoneally treated with saline (control) or flupirtine at various doses (1-10 mg/kg) and time-points (0-12 hours). Tissue survival and cell signaling were studied on day 2, whereas neurological recovery and tissue remodeling were analyzed until day 84. Flupirtine induced sustained neuroprotection, when delivered up to 9 hours. The latter yielded enhanced neurological recovery that persisted over three months and which was accompanied by enhanced angioneurogenesis. On the molecular level, inhibition of calpain activation was noted, which was associated with increased signal-transducer-and-activator-of-transcription-6 (STAT6) abundance, reduced N-terminal-Jun-kinase and NF-kappa B activation, as well as reduced proteasomal activity. Consequently, blood-brain-barrier integrity was stabilized, oxidative stress was reduced and brain leukocyte infiltration was diminished. In view of its excellent tolerability, considering its sustained effects on neurological recovery, brain tissue survival and remodeling, flupirtine is an attractive candidate for stroke therapy."],["dc.identifier.doi","10.18632/oncotarget.4226"],["dc.identifier.gro","3141888"],["dc.identifier.isi","000359010000019"],["dc.identifier.pmid","26050199"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12677"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2189"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: TUBITAK [2221]; German Research Council [HE3173/2-2, HE3173/3-1]"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.subject","pathology; excitotoxicity; focal cerebral ischemia; neuroprotection; N-methyl-D-aspartate-receptors (NMDAR)"],["dc.title","The indirect NMDAR inhibitor flupirtine induces sustained post-ischemic recovery, neuroprotection and angioneurogenesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]