Venkataramani, Vivek

[["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.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.artnumber","1068"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Cell Death & Disease"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Zhang, Lin"],["dc.contributor.author","Wei, Wei"],["dc.contributor.author","Ai, Xiaoyu"],["dc.contributor.author","Kilic, Ertugrul"],["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","2021-12-01T09:20:49Z"],["dc.date.available","2021-12-01T09:20:49Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract Systemic transplantation of oxygen−glucose deprivation (OGD)-preconditioned primary microglia enhances neurological recovery in rodent stroke models, albeit the underlying mechanisms have not been sufficiently addressed. Herein, we analyzed whether or not extracellular vesicles (EVs) derived from such microglia are the biological mediators of these observations and which signaling pathways are involved in the process. Exposing bEnd.3 endothelial cells (ECs) and primary cortical neurons to OGD, the impact of EVs from OGD-preconditioned microglia on angiogenesis and neuronal apoptosis by the tube formation assay and TUNEL staining was assessed. Under these conditions, EV treatment stimulated both angiogenesis and tube formation in ECs and repressed neuronal cell injury. Characterizing microglia EVs by means of Western blot analysis and other techniques revealed these EVs to be rich in TGF-β1. The latter turned out to be a key compound for the therapeutic potential of microglia EVs, affecting the Smad2/3 pathway in both ECs and neurons. EV infusion in stroke mice confirmed the aforementioned in vitro results, demonstrating an activation of the TGF-β/Smad2/3 signaling pathway within the ischemic brain. Furthermore, enriched TGF-β1 in EVs secreted from OGD-preconditioned microglia stimulated M2 polarization of residing microglia within the ischemic cerebral environment, which may contribute to a regulation of an early inflammatory response in postischemic hemispheres. These observations are not only interesting from the mechanistic point of view but have an immediate therapeutic implication as well, since stroke mice treated with such EVs displayed a better functional recovery in the behavioral test analyses. Hence, the present findings suggest a new way of action of EVs derived from OGD-preconditioned microglia by regulating the TGF-β/Smad2/3 pathway in order to promote tissue regeneration and neurological recovery in stroke mice."],["dc.description.abstract","Abstract Systemic transplantation of oxygen−glucose deprivation (OGD)-preconditioned primary microglia enhances neurological recovery in rodent stroke models, albeit the underlying mechanisms have not been sufficiently addressed. Herein, we analyzed whether or not extracellular vesicles (EVs) derived from such microglia are the biological mediators of these observations and which signaling pathways are involved in the process. Exposing bEnd.3 endothelial cells (ECs) and primary cortical neurons to OGD, the impact of EVs from OGD-preconditioned microglia on angiogenesis and neuronal apoptosis by the tube formation assay and TUNEL staining was assessed. Under these conditions, EV treatment stimulated both angiogenesis and tube formation in ECs and repressed neuronal cell injury. Characterizing microglia EVs by means of Western blot analysis and other techniques revealed these EVs to be rich in TGF-β1. The latter turned out to be a key compound for the therapeutic potential of microglia EVs, affecting the Smad2/3 pathway in both ECs and neurons. EV infusion in stroke mice confirmed the aforementioned in vitro results, demonstrating an activation of the TGF-β/Smad2/3 signaling pathway within the ischemic brain. Furthermore, enriched TGF-β1 in EVs secreted from OGD-preconditioned microglia stimulated M2 polarization of residing microglia within the ischemic cerebral environment, which may contribute to a regulation of an early inflammatory response in postischemic hemispheres. These observations are not only interesting from the mechanistic point of view but have an immediate therapeutic implication as well, since stroke mice treated with such EVs displayed a better functional recovery in the behavioral test analyses. Hence, the present findings suggest a new way of action of EVs derived from OGD-preconditioned microglia by regulating the TGF-β/Smad2/3 pathway in order to promote tissue regeneration and neurological recovery in stroke mice."],["dc.identifier.doi","10.1038/s41419-021-04363-7"],["dc.identifier.pii","4363"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94280"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","2041-4889"],["dc.title","Extracellular vesicles from hypoxia-preconditioned microglia promote angiogenesis and repress apoptosis in stroke mice via the TGF-β/Smad2/3 pathway"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]