Options
Venkataramani, Vivek
Loading...
Preferred name
Venkataramani, Vivek
Official Name
Venkataramani, Vivek
Alternative Name
Venkataramani, V.
Main Affiliation
Now showing 1 - 10 of 31
2016Journal Article Research Paper [["dc.bibliographiccitation.firstpage","395"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Clinical Cancer Research"],["dc.bibliographiccitation.lastpage","404"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Koch, Raphael"],["dc.contributor.author","Aung, Thiha"],["dc.contributor.author","Vogel, Daniel"],["dc.contributor.author","Chapuy, Björn"],["dc.contributor.author","Wenzel, Dirk"],["dc.contributor.author","Becker, Sabrina"],["dc.contributor.author","Sinzig, Ursula"],["dc.contributor.author","Venkataramani, Vivek"],["dc.contributor.author","von Mach, Tobias"],["dc.contributor.author","Jacob, Ralf"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Wulf, Gerald G."],["dc.date.accessioned","2018-11-07T10:19:22Z"],["dc.date.available","2018-11-07T10:19:22Z"],["dc.date.issued","2016"],["dc.description.abstract","Purpose: Although R-CHOP-based immunochemotherapy cures significant proportions of patients with aggressive B-cell lymphoma, tumor cell susceptibility to chemotherapy varies, with mostly fatal outcome in cases of resistant disease. We and others have shown before that export of cytostatic drugs contributes to drug resistance. Now we provide a novel approach to overcome exosome-mediated drug resistance in aggressive B-cell lymphomas. Experimental Design: We used well-established centrifugation protocols to purify exosomes from DLBCL cell lines and detected anthracyclines using FACS and HPLC. We used shRNA knockdown of ABCA3 to determine ABCA3 dependence of chemotherapy susceptibility and monitored ABCA3 expression after indomethacin treatment using qPCR. Finally, we established an in vivo assay using a chorioallantoic membrane (CAM) assay to determine the synergy of anthracycline and indomethacin treatment. Results: We show increased efficacy of the anthracycline doxorubicin and the anthracenedione pixantrone by suppression of exosomal drug resistance with indomethacin. B-cell lymphoma cells in vitro efficiently extruded doxorubicin and pixantrone, in part compacted in exosomes. Exosomal biogenesis was critically dependent on the expression of the ATP-transporter A3 (ABCA3). Genetic or chemical depletion of ABCA3 augmented intracellular retention of both drugs and shifted the subcellular drug accumulation to prolonged nuclear retention. Indomethacin increased the cytostatic efficacy of both drugs against DLBCL cell lines in vitro and in vivo in a CAM assay. Conclusions: We propose pretreatment with indomethacin toward enhanced antitumor efficacy of anthracyclines and anthracenediones. (C) 2015 AACR."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft; University Medicine Goettingen"],["dc.identifier.doi","10.1158/1078-0432.CCR-15-0577"],["dc.identifier.isi","000369076500016"],["dc.identifier.pmid","26369630"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41643"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1557-3265"],["dc.relation.issn","1078-0432"],["dc.title","Nuclear Trapping through Inhibition of Exosomal Export by Indomethacin Increases Cytostatic Efficacy of Doxorubicin and Pixantrone"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2019Journal Article [["dc.bibliographiccitation.firstpage","833"],["dc.bibliographiccitation.journal","Toxicology Reports"],["dc.bibliographiccitation.lastpage","840"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Akinyemi, Ayodele Jacob"],["dc.contributor.author","Miah, Mahfuzur R."],["dc.contributor.author","Ijomone, Omamuyovwi M."],["dc.contributor.author","Tsatsakis, Aristidis"],["dc.contributor.author","Soares, Félix Alexandre Antunes"],["dc.contributor.author","Tinkov, Alexey A."],["dc.contributor.author","Skalny, Anatoly V."],["dc.contributor.author","Venkataramani, Vivek"],["dc.contributor.author","Aschner, Michael"],["dc.date.accessioned","2020-12-10T15:21:37Z"],["dc.date.available","2020-12-10T15:21:37Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1016/j.toxrep.2019.08.001"],["dc.identifier.issn","2214-7500"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73092"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Lead (Pb) exposure induces dopaminergic neurotoxicity in Caenorhabditis elegans: Involvement of the dopamine transporter"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2020Journal Article [["dc.bibliographiccitation.firstpage","108357"],["dc.bibliographiccitation.journal","Neuropharmacology"],["dc.bibliographiccitation.volume","181"],["dc.contributor.author","Haupt, Matteo"],["dc.contributor.author","Zechmeister, Bozena"],["dc.contributor.author","Bosche, Bert"],["dc.contributor.author","Lieschke, Simone"],["dc.contributor.author","Zheng, Xuan"],["dc.contributor.author","Zhang, Lin"],["dc.contributor.author","Venkataramani, Vivek"],["dc.contributor.author","Jin, Fengyan"],["dc.contributor.author","Hein, Katharina"],["dc.contributor.author","Doeppner, Thorsten R."],["dc.date.accessioned","2021-06-01T09:41:26Z"],["dc.date.available","2021-06-01T09:41:26Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1016/j.neuropharm.2020.108357"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84920"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.issn","0028-3908"],["dc.title","Lithium enhances post-stroke blood-brain barrier integrity, activates the MAPK/ERK1/2 pathway and alters immune cell migration in mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2021Journal Article [["dc.bibliographiccitation.firstpage","313"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Nature Microbiology"],["dc.bibliographiccitation.lastpage","326"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Soliman, Sameh S. M."],["dc.contributor.author","Baldin, Clara"],["dc.contributor.author","Gu, Yiyou"],["dc.contributor.author","Singh, Shakti"],["dc.contributor.author","Gebremariam, Teclegiorgis"],["dc.contributor.author","Swidergall, Marc"],["dc.contributor.author","Alqarihi, Abdullah"],["dc.contributor.author","Youssef, Eman G."],["dc.contributor.author","Alkhazraji, Sondus"],["dc.contributor.author","Pikoulas, Antonis"],["dc.contributor.author","Perske, Christina"],["dc.contributor.author","Venkataramani, Vivek"],["dc.contributor.author","Rich, Abigail"],["dc.contributor.author","Bruno, Vincent M."],["dc.contributor.author","Hotopp, Julie Dunning"],["dc.contributor.author","Mantis, Nicolas J."],["dc.contributor.author","Edwards, John E."],["dc.contributor.author","Filler, Scott G."],["dc.contributor.author","Chamilos, Georgios"],["dc.contributor.author","Vitetta, Ellen S."],["dc.contributor.author","Ibrahim, Ashraf S."],["dc.date.accessioned","2021-04-14T08:30:18Z"],["dc.date.available","2021-04-14T08:30:18Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1038/s41564-020-00837-0"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83181"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","2058-5276"],["dc.title","Mucoricin is a ricin-like toxin that is critical for the pathogenesis of mucormycosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2021Journal Article [["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"]]Details DOI2019Journal Article [["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"]]Details DOI2013Conference Abstract [["dc.bibliographiccitation.journal","Onkologie"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Venkataramani, Vivek"],["dc.contributor.author","Aung, T."],["dc.contributor.author","Kiecke, Christina"],["dc.contributor.author","Kueffer, Stefan"],["dc.contributor.author","Stroebel, Philipp"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Wulf, Gerald G."],["dc.date.accessioned","2018-11-07T09:19:02Z"],["dc.date.available","2018-11-07T09:19:02Z"],["dc.date.issued","2013"],["dc.format.extent","20"],["dc.identifier.isi","000326360900043"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28544"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.publisher.place","Basel"],["dc.relation.issn","1423-0240"],["dc.relation.issn","0378-584X"],["dc.title","The biological relevance of the Amyloid Precursor Protein (APP) in prostate cancer"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS2013Journal Article [["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"]]Details DOI PMID PMC WOS2018Journal Article [["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"]]Details DOI2012Conference Abstract [["dc.bibliographiccitation.journal","Onkologie"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Venkataramani, Vivek"],["dc.contributor.author","Behnes, Carl Ludwig"],["dc.contributor.author","Thiele, K."],["dc.contributor.author","Wulf, Gerald G."],["dc.contributor.author","Thelen, F."],["dc.contributor.author","Opitz, Lennart"],["dc.contributor.author","Salinas-Riester, Gabriela"],["dc.contributor.author","Wirths, Oliver"],["dc.contributor.author","Bayer, Thomas A."],["dc.contributor.author","Schweyer, Stefan"],["dc.date.accessioned","2018-11-07T09:04:55Z"],["dc.date.available","2018-11-07T09:04:55Z"],["dc.date.issued","2012"],["dc.format.extent","195"],["dc.identifier.isi","000310766700509"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25208"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.publisher.place","Basel"],["dc.relation.issn","0378-584X"],["dc.title","The Alzheimer Amyloid Precursor Protein (APP) is a biomarker for transformed human pluripotent stem cells - from Alzheimer's disease to cancer biology and beyond"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS