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.firstpage","3546"],["dc.bibliographiccitation.issue","19"],["dc.bibliographiccitation.journal","International Journal of Environmental Research and Public Health"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Martins, Airton Cunha"],["dc.contributor.author","Morcillo, Patricia"],["dc.contributor.author","Ijomone, Omamuyovwi Meashack"],["dc.contributor.author","Venkataramani, Vivek"],["dc.contributor.author","Harrison, Fiona Edith"],["dc.contributor.author","Lee, Eunsook"],["dc.contributor.author","Bowman, Aaron Blaine"],["dc.contributor.author","Aschner, Michael"],["dc.date.accessioned","2020-12-10T18:47:07Z"],["dc.date.available","2020-12-10T18:47:07Z"],["dc.date.issued","2019"],["dc.description.sponsorship","National Institute of Environmental Health Sciences"],["dc.identifier.doi","10.3390/ijerph16193546"],["dc.identifier.eissn","1660-4601"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16959"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78650"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","MDPI"],["dc.relation.eissn","1660-4601"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","New Insights on the Role of Manganese in Alzheimer’s Disease and Parkinson’s Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1385"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","International Journal of Oncology"],["dc.bibliographiccitation.lastpage","1394"],["dc.bibliographiccitation.volume","43"],["dc.contributor.author","Hasibeder, Astrid"],["dc.contributor.author","Venkataramani, Vivek"],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Radzun, Heinz-Joachim"],["dc.contributor.author","Schweyer, Stefan"],["dc.date.accessioned","2018-11-07T09:18:23Z"],["dc.date.available","2018-11-07T09:18:23Z"],["dc.date.issued","2013"],["dc.description.abstract","Phytoestrogens have been shown to exert antiproliferative effects on different cancer cells. In addition it could be demonstrated that inhibition of proliferation is associated with downregulation of the known stem cell factors NANOG, POU5F1 and SOX2 in tumor cells. We demonstrate the potential of Belamcanda chinensis extract (BCE) and tectorigenin as anticancer drugs in cell lines of malignant testicular germ cell tumor cells (TGCT) by inhibition of proliferation and regulating the expression of stem cell factors. The TGCT cell lines TCam-2 and NTera-2 were treated with BCE or tectorigenin and MTT assay was used to measure the proliferation of tumor cells. In addition, the expression of stem cell factors was analyzed by quantitative PCR and western blot analysis. Furthermore, global expression analysis was performed by microarray technique. BCE and tectorigenin inhibited proliferation and downregulated the stem cell factors NANOG and POU5F1 in TGCT cells. In addition, gene expression profiling revealed induction of genes important for the differentiation and inhibition of oncogenes. Utilizing connectivity map in an attempt to elucidate mechanism underlying BCE treatments we found highly positive association to histone deacetylase inhibitors (HDACi) amongst others. Causing no histone deacetylase inhibition, the effects of BCE on proliferation and stem cell factors may be based on histone-independent mechanisms such as direct hyperacetylation of transcription factors. Based on these findings, phytoestrogens may be useful as new agents in the treatment of TGCT."],["dc.identifier.doi","10.3892/ijo.2013.2060"],["dc.identifier.isi","000324982700007"],["dc.identifier.pmid","23969837"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9295"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28398"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Spandidos Publ Ltd"],["dc.relation.issn","1019-6439"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Phytoestrogens regulate the proliferation and expression of stem cell factors in cell lines of malignant testicular germ cell tumors"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","10678"],["dc.bibliographiccitation.issue","14"],["dc.bibliographiccitation.journal","Journal of Biological Chemistry"],["dc.bibliographiccitation.lastpage","10689"],["dc.bibliographiccitation.volume","285"],["dc.contributor.author","Venkataramani, Vivek"],["dc.contributor.author","Rossner, Christian"],["dc.contributor.author","Iffland, Lara"],["dc.contributor.author","Schweyer, Stefan"],["dc.contributor.author","Tamboli, Irfan Y."],["dc.contributor.author","Walter, Jochen"],["dc.contributor.author","Wirths, Oliver"],["dc.contributor.author","Bayer, Thomas A."],["dc.date.accessioned","2018-11-07T08:44:13Z"],["dc.date.available","2018-11-07T08:44:13Z"],["dc.date.issued","2010"],["dc.description.abstract","The beta-amyloid precursor protein (APP) represents a type I transmembrane glycoprotein that is ubiquitously expressed. In the brain, it is a key player in the molecular pathogenesis of Alzheimer disease. Its physiological function is however less well understood. Previous studies showed that APP is up-regulated in prostate, colon, pancreatic tumor, and oral squamous cell carcinoma. In this study, we show that APP has an essential role in growth control of pancreatic and colon cancer. Abundant APP staining was found in human pancreatic adenocarcinoma and colon cancer tissue. Interestingly, treating pancreatic and colon cancer cells with valproic acid (VPA, 2-propylpentanoic acid), a known histone deacetylase (HDAC) inhibitor, leads to up-regulation of GRP78, an endoplasmic reticulum chaperone immunoglobulin-binding protein. GRP78 is involved in APP maturation and inhibition of tumor cell growth by down-regulation of APP and secreted soluble APP alpha. Trichostatin A, a pan-HDAC inhibitor, also lowered APP and increased GRP78 levels. In contrast, treating cells with valpromide, a VPA derivative lacking HDAC inhibitory properties, had no effect on APP levels. VPA did not modify the level of epidermal growth factor receptor, another type I transmembrane protein, and APLP2, a member of the APP family, demonstrating the specificity of the VPA effect on APP. Small interfering RNA-mediated knockdown of APP also resulted in significantly decreased cell growth. Based on these observations, the data suggest that APP downregulation via HDAC inhibition provides a novel mechanism for pancreatic and colon cancer therapy."],["dc.identifier.doi","10.1074/jbc.M109.057836"],["dc.identifier.isi","000276264600055"],["dc.identifier.pmid","20145244"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6302"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20148"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Biochemistry Molecular Biology Inc"],["dc.relation.issn","0021-9258"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Histone Deacetylase Inhibitor Valproic Acid Inhibits Cancer Cell Proliferation via Down-regulation of the Alzheimer Amyloid Precursor Protein"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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.journal","Translational Stroke Research"],["dc.contributor.author","Zheng, X."],["dc.contributor.author","Zhang, L."],["dc.contributor.author","Kuang, Y."],["dc.contributor.author","Venkataramani, V."],["dc.contributor.author","Jin, F."],["dc.contributor.author","Hein, K."],["dc.contributor.author","Zafeiriou, M. P."],["dc.contributor.author","Lenz, C."],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Kilic, E."],["dc.contributor.author","Hermann, D. M."],["dc.contributor.author","Weber, M. S."],["dc.contributor.author","Urlaub, H."],["dc.contributor.author","Zimmermann, W.-H."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Doeppner, Thorsten R."],["dc.date.accessioned","2020-12-10T14:14:38Z"],["dc.date.available","2020-12-10T14:14:38Z"],["dc.date.issued","2020"],["dc.description.abstract","Stem cells such as mesenchymal stem cells (MSCs) enhance neurological recovery in preclinical stroke models by secreting extracellular vesicles (EVs). Since previous reports have focused on the application of MSC-EVs only, the role of the most suitable host cell for EV enrichment and preclinical stroke treatment remains elusive. The present study aimed to evaluate the therapeutic potential of EVs derived from neural progenitor cells (NPCs) following experimental stroke. Using the PEG technique, EVs were enriched and characterized by electron microscopy, proteomics, rt-PCR, nanosight tracking analysis, and Western blotting. Different dosages of NPC-EVs displaying a characteristic profile in size, shape, cargo protein, and non-coding RNA contents were incubated in the presence of cerebral organoids exposed to oxygen-glucose deprivation (OGD), significantly reducing cell injury when compared with control organoids. Systemic administration of NPC-EVs in male C57BL6 mice following experimental ischemia enhanced neurological recovery and neuroregeneration for as long as 3 months. Interestingly, the therapeutic impact of such NPC-EVs was found to be not inferior to MSC-EVs. Flow cytometric analyses of blood and brain samples 7 days post-stroke demonstrated increased blood concentrations of B and T lymphocytes after NPC-EV delivery, without affecting cerebral cell counts. Likewise, a biodistribution analysis after systemic delivery of NPC-EVs revealed the majority of NPC-EVs to be found in extracranial organs such as the liver and the lung. This proof-of-concept study supports the idea of EVs being a general concept of stem cell–induced neuroprotection under stroke conditions, where EVs contribute to reverting the peripheral post-stroke immunosuppression."],["dc.identifier.doi","10.1007/s12975-020-00814-z"],["dc.identifier.pmid","32361827"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71426"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/42"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/354"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.haserratum","/handle/2/94655"],["dc.relation.workinggroup","RG Bähr (Neurobiological Research Laboratory)"],["dc.relation.workinggroup","RG Möbius"],["dc.relation.workinggroup","RG Zafeiriou (3D Electrically Excitable Cell Networks – Brain and Heart)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.relation.workinggroup","RG Lenz"],["dc.rights","CC BY 4.0"],["dc.title","Extracellular Vesicles Derived from Neural Progenitor Cells––a Preclinical Evaluation for Stroke Treatment 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.firstpage","1636"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The American Journal of Pathology"],["dc.bibliographiccitation.lastpage","1652"],["dc.bibliographiccitation.volume","180"],["dc.contributor.author","Venkataramani, Vivek"],["dc.contributor.author","Thiele, Knut"],["dc.contributor.author","Behnes, Carl Ludwig"],["dc.contributor.author","Wulf, Gerald G."],["dc.contributor.author","Thelen, Paul"],["dc.contributor.author","Opitz, Lennart"],["dc.contributor.author","Salinas-Riester, Gabriella"],["dc.contributor.author","Wirths, Oliver"],["dc.contributor.author","Bayer, Thomas A."],["dc.contributor.author","Schweyer, Stefan"],["dc.date.accessioned","2019-07-09T11:54:33Z"],["dc.date.available","2019-07-09T11:54:33Z"],["dc.date.issued","2012"],["dc.description.abstract","Increasing evidence suggests an important function of the -amyloid precursor protein (APP) in malignant disease in humans; however, the biological basis for this evidence is not well understood at present. To understand the role of APP in transformed pluripotent stem cells, we studied its expression levels in human testicular germ cell tumors using patient tissues, model cell lines, and an established xenograft mouse model. In the present study, we demonstrate the cooperative expression of APP with prominent pluripotency-related genes such as Sox2, NANOG, and POU5F1 (Oct3/4). The closest homologue family member, APLP2, showed no correlation to these stem cell factors. In addition, treatment with histone deacetylase (HDAC) inhibitors suppressed the levels of APP and stem cell markers. Loss of pluripotency, either spontaneously or as a consequence of treatment with an HDAC inhibitor, was accompanied by decreased APP protein levels both in vitro and in vivo. These observations suggest that APP represents a novel and specific biomarker in human transformed pluripotent stem cells that can be selectively modulated by HDAC inhibitors."],["dc.identifier.doi","10.1016/j.ajpath.2011.12.015"],["dc.identifier.fs","584577"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9289"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60677"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Amyloid Precursor Protein Is a Biomarker for Transformed Human Pluripotent Stem Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]