Sirén, Anna-Leena

[["dc.bibliographiccitation.firstpage","217"],["dc.bibliographiccitation.lastpage","236"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Krampe, Henning"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.contributor.editor","Felthous, Alan"],["dc.contributor.editor","Sass, Henning"],["dc.date.accessioned","2017-09-07T11:46:20Z"],["dc.date.available","2017-09-07T11:46:20Z"],["dc.date.issued","2008"],["dc.identifier.gro","3150480"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7249"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.publisher","Wiley"],["dc.publisher.place","Chichester"],["dc.relation.isbn","978-0-470-01185-0"],["dc.relation.ispartof","The International Handbook of Psychopathic Disorders and the Law, Vol. 1"],["dc.title","Brain trauma"],["dc.type","book_chapter"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","427"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Cerebral Blood Flow and Metabolism"],["dc.bibliographiccitation.lastpage","430"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Heyer, Andrea"],["dc.contributor.author","Hasselblatt, Martin"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Häfner, Heinz"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:18Z"],["dc.date.available","2017-09-07T11:46:18Z"],["dc.date.issued","2005"],["dc.description.abstract","Gender differences in neuropsychiatric disease are recognized but not well understood. Investigating the survival of primary rat hippocampal neurons in culture, we found significant and inverted gender differences on normoxia versus hypoxia. Male cells were more resistant under normoxia but more vulnerable under hypoxia than female cells. Male vulnerability pattern was acquired in cells from neonatally testosterone-primed females. Estrogens, acting via membrane receptors, had a higher neuroprotective power in male neurons, explained at least in part by the pronounced increase in estrogen receptor beta/alpha ratio during hypoxia in male cells only."],["dc.identifier.doi","10.1038/sj.jcbfm.9600056"],["dc.identifier.gro","3150469"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7237"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","0271-678X"],["dc.subject","aromatase; estrogen receptor alpha; estrogen receptor beta; hippocampus; sex; testosterone"],["dc.title","In vitro gender differences in neuronal survival on hypoxia and in 17 beta-estradiol-mediated neuroprotection"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","eaax9070"],["dc.bibliographiccitation.issue","26"],["dc.bibliographiccitation.journal","Science Advances"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Koster, Jeremy"],["dc.contributor.author","McElreath, Richard"],["dc.contributor.author","Hill, Kim"],["dc.contributor.author","Yu, Douglas"],["dc.contributor.author","Shepard, Glenn"],["dc.contributor.author","van Vliet, Nathalie"],["dc.contributor.author","Gurven, Michael"],["dc.contributor.author","Trumble, Benjamin"],["dc.contributor.author","Bird, Rebecca Bliege"],["dc.contributor.author","Bird, Douglas"],["dc.contributor.author","Codding, Brian"],["dc.contributor.author","Coad, Lauren"],["dc.contributor.author","Pacheco-Cobos, Luis"],["dc.contributor.author","Winterhalder, Bruce"],["dc.contributor.author","Lupo, Karen"],["dc.contributor.author","Schmitt, Dave"],["dc.contributor.author","Sillitoe, Paul"],["dc.contributor.author","Franzen, Margaret"],["dc.contributor.author","Alvard, Michael"],["dc.contributor.author","Venkataraman, Vivek"],["dc.contributor.author","Kraft, Thomas"],["dc.contributor.author","Endicott, Kirk"],["dc.contributor.author","Beckerman, Stephen"],["dc.contributor.author","Marks, Stuart A."],["dc.contributor.author","Headland, Thomas"],["dc.contributor.author","Pangau-Adam, Margaretha"],["dc.contributor.author","Siren, Anders"],["dc.contributor.author","Kramer, Karen"],["dc.contributor.author","Greaves, Russell"],["dc.contributor.author","Reyes-García, Victoria"],["dc.contributor.author","Guèze, Maximilien"],["dc.contributor.author","Duda, Romain"],["dc.contributor.author","Fernández-Llamazares, Álvaro"],["dc.contributor.author","Gallois, Sandrine"],["dc.contributor.author","Napitupulu, Lucentezza"],["dc.contributor.author","Ellen, Roy"],["dc.contributor.author","Ziker, John"],["dc.contributor.author","Nielsen, Martin R."],["dc.contributor.author","Ready, Elspeth"],["dc.contributor.author","Healey, Christopher"],["dc.contributor.author","Ross, Cody"],["dc.date.accessioned","2021-04-14T08:25:22Z"],["dc.date.available","2021-04-14T08:25:22Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1126/sciadv.aax9070"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81605"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","2375-2548"],["dc.title","The life history of human foraging: Cross-cultural and individual variation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","154"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Cellular Signalling"],["dc.bibliographiccitation.lastpage","162"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Samoylenko, Anatoly"],["dc.contributor.author","Byts, Nadiya"],["dc.contributor.author","Rajalingam, Krishnaraj"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Rapp, Ulf R."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.date.accessioned","2017-09-07T11:46:16Z"],["dc.date.available","2017-09-07T11:46:16Z"],["dc.date.issued","2008-01"],["dc.description.abstract","Thrombopoietin (TPO), a hematopoietic growth factor regulating platelet production, and its receptor (TPOR) were recently shown to be expressed in the brain where they exert proapoptotic activity. Here we used PC12 cells, an established model of neuronal differentiation, to investigate the effects of TPO on neuronal survival and differentiation. These cells expressed TPOR mRNA. TPO increased cell death in neuronally differentiated PC12 cells but had no effect in undifferentiated cells. Surprisingly, TPO inhibited nerve growth factor (NGF)-induced differentiation of PC12 cells in a dose- and time-dependent manner. This inhibition was dependent on the activity of Janus kinase-2 (JAK2). Using phospho-kinase arrays and Western blot we found downregulation of the NGF-stimulated phosphorylation of the extracellular signal-regulated kinase p42ERK by TPO with no effect on phosphorylation of Akt or stress kinases. NGF-induced phosphorylation of ERK-activating kinases, MEK1/2 and C-RAF was also reduced by TPO while NGF-induced RAS activation was not attenuated by TPO treatment. In contrast to its inhibitory effects on NGF signalling, TPO had no effect on epidermal growth factor (EGF)-stimulated ERK phosphorylation or proliferation of PC12 cells. Our data indicate that TPO via activation of its receptor-bound JAK2 delays the NGF-dependent acquisition of neuronal phenotype and decreases neuronal survival by suppressing NGF-induced ERK activity."],["dc.identifier.doi","10.1016/j.cellsig.2007.10.006"],["dc.identifier.gro","3150475"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7244"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.subject","TPO; NGF; EGF; PC12; RAS; Mitogen-activated protein kinase; Cell death; Neurite outgrowth"],["dc.title","Thrombopoietin inhibits nerve growth factor-induced neuronal differentiation and ERK signalling"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1305"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Neurochemical Research"],["dc.bibliographiccitation.lastpage","1309"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Unzicker, Christian"],["dc.contributor.author","Erberich, Heike"],["dc.contributor.author","Moldrich, Gabriella"],["dc.contributor.author","Woldt, Helge"],["dc.contributor.author","Bulla, Jan"],["dc.contributor.author","Mechoulam, Raphael"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.date.accessioned","2017-09-07T11:46:33Z"],["dc.date.available","2017-09-07T11:46:33Z"],["dc.date.issued","2005"],["dc.description.abstract","Endothelin (ETB)-receptors mediate anti-apoptotic actions. Lack of functional ETB-receptors leads to increased neuronal apoptosis in the hippocampus. The increased apoptosis must be compensated by other mechanisms, however, as ETB-deficient rats display normal overall brain morphology. To illuminate on brain plasticity in ETB-receptor deficiency, we studied the expression and function of another neuroprotective system, the cannabinoid CB1-receptors, in ETB-deficient hippocampus. We show that CB1 expression in hippocampus increases postnatally in all rats but that the increase in CB1-receptor expression is significantly higher in ETB-deficient compared to wildtype littermates. Neuronal apoptosis decreases during brain maturation but remains on a significantly higher level in the ETB-deficient compared to wildtype dentate. When investigating survival of hippocampal neurons in culture, we found significant protection against hypoxia-induced cell death with CB1-analogs (noladin, (9-tetrahydrocannabinol) only in ETB-deficient neurons. We suggest that CB1-receptor upregulation in the ETB-mutant hippocampus reflects an attempt to compensate for the lack of ETB-receptors."],["dc.identifier.doi","10.1007/s11064-005-8802-3"],["dc.identifier.gro","3150522"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7294"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.subject","Cannabis; CB1; endocannabinoid system; noladin; tetrahydrocannabinol; THC; endothelin; ETB; apoptosis; hippocampus; dentate gyrus; neuronal culture; Wistar-Imamichi rat; spotting lethal rat; hypoxia; neuroprotection; immunohistochemistry; Western blot"],["dc.title","Hippocampal cannabinoid-1 receptor upregulation upon endothelin-B receptor deficiency: A neuroprotective substitution effect?"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1219"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Neurochemical Research"],["dc.bibliographiccitation.lastpage","1230"],["dc.contributor.author","Byts, Nadiya"],["dc.contributor.author","Samoylenko, Anatoly"],["dc.contributor.author","Woldt, Helge"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.date.accessioned","2017-09-07T11:46:18Z"],["dc.date.available","2017-09-07T11:46:18Z"],["dc.date.issued","2006"],["dc.description.abstract","Correct timing and spatial location of growth factor expression is critical for undisturbed brain development and functioning. In terminally differentiated cells distinct biological responses to growth factors may depend on cell type specific activation of signalling cascades. We show that the hematopoietic growth factors thrombopoietin (TPO) and granulocyte colony-stimulating factor (GCSF) exert cell type specific effects on survival, proliferation and the degree of phosphorylation of Akt1, ERK1/2 and STAT3 in rat hippocampal neurons and cortical astrocytes. In neurons, TPO induced cell death and selectively activated ERK1/2. GCSF protected neurons from TPO- and hypoxia-induced cell death via selective activation of Akt1. In astrocytes, neither TPO nor GCSF had any effect on cell viability but inhibited proliferation. This effect was accompanied by activation of ERK1/2 and inhibition of STAT3 activity. A balance between growth factors, their receptors and signalling proteins may play an important role in regulation of neural cell survival."],["dc.identifier.gro","3150471"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7239"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.relation.issn","0364-3190"],["dc.title","Cell type specific signalling by hematopoietic growth factors in neural cells"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4044"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences of the United States of America"],["dc.bibliographiccitation.lastpage","4049"],["dc.bibliographiccitation.volume","98"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.contributor.author","Fratelli, Maddalena"],["dc.contributor.author","Brines, Michael"],["dc.contributor.author","Goemans, Christoph"],["dc.contributor.author","Casagrande, Simona"],["dc.contributor.author","Lewczuk, Pjotr"],["dc.contributor.author","Keenan, Sonja"],["dc.contributor.author","Gleiter, Christoph H."],["dc.contributor.author","Pasquali, Claudio"],["dc.contributor.author","Capobianco, Annalisa"],["dc.contributor.author","Mennini, Tiziana"],["dc.contributor.author","Heumann, Rolf"],["dc.contributor.author","Cerami, Anthony"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Ghezzi, Pietro"],["dc.date.accessioned","2018-03-08T09:22:11Z"],["dc.date.available","2018-03-08T09:22:11Z"],["dc.date.issued","2001"],["dc.description.abstract","Erythropoietin (EPO) promotes neuronal survival after hypoxia and other metabolic insults by largely unknown mechanisms. Apoptosis and necrosis have been proposed as mechanisms of cellular demise, and either could be the target of actions of EPO. This study evaluates whether antiapoptotic mechanisms can account for the neuroprotective actions of EPO. Systemic administration of EPO (5,000 units/kg of body weight, i.p.) after middle-cerebral artery occlusion in rats dramatically reduces the volume of infarction 24 h later, in concert with an almost complete reduction in the number of terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling of neurons within the ischemic penumbra. In both pure and mixed neuronal cultures, EPO (0.1–10 units/ml) also inhibits apoptosis induced by serum deprivation or kainic acid exposure. Protection requires pretreatment, consistent with the induction of a gene expression program, and is sustained for 3 days without the continued presence of EPO. EPO (0.3 units/ml) also protects hippocampal neurons against hypoxia-induced neuronal death through activation of extracellular signal-regulated kinases and protein kinase Akt-1/protein kinase B. The action of EPO is not limited to directly promoting cell survival, as EPO is trophic but not mitogenic in cultured neuronal cells. These data suggest that inhibition of neuronal apoptosis underlies short latency protective effects of EPO after cerebral ischemia and other brain injuries. The neurotrophic actions suggest there may be longer-latency effects as well. Evaluation of EPO, a compound established as clinically safe, as neuroprotective therapy in acute brain injury is further supported."],["dc.identifier.doi","10.1073/pnas.051606598"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/12910"],["dc.language.iso","en"],["dc.notes.intern","GRO-Li-Import"],["dc.notes.status","final"],["dc.relation.doi","10.1073/pnas.051606598"],["dc.relation.issn","0027-8424"],["dc.relation.issn","1091-6490"],["dc.title","Erythropoietin prevents neuronal apoptosis after cerebral ischemia and metabolic stress"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","111"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Georgia Augusta"],["dc.bibliographiccitation.lastpage","115"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.date.accessioned","2017-09-07T11:45:45Z"],["dc.date.available","2017-09-07T11:45:45Z"],["dc.date.issued","2003"],["dc.identifier.gro","3150433"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7196"],["dc.language.iso","de"],["dc.notes.status","zu prüfen"],["dc.title","EPO - Neuroprotektion bei Hirnerkrankungen"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","186"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Pineal Research"],["dc.bibliographiccitation.lastpage","187"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Jacob, Sonja"],["dc.contributor.author","Poeggeler, Burkhard"],["dc.contributor.author","Weishaupt, Jochen H."],["dc.contributor.author","Sirén, Anna-Leena"],["dc.contributor.author","Hardeland, Rüdiger"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:45:41Z"],["dc.date.available","2017-09-07T11:45:41Z"],["dc.date.issued","2002"],["dc.identifier.doi","10.1034/j.1600-079X.2002.02943.x"],["dc.identifier.gro","3150431"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7194"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","0742-3098"],["dc.title","Melatonin as a candidate compound for neuroprotection in amyotrophic lateral sclerosis (ALS): high tolerability of daily oral melatonin administration in ALS patients"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","108"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neurotherapeutics"],["dc.bibliographiccitation.lastpage","127"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.contributor.author","Faßhauer, Theresa"],["dc.contributor.author","Bartels, Claudia"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:45:45Z"],["dc.date.available","2017-09-07T11:45:45Z"],["dc.date.issued","2009"],["dc.description.abstract","The growth factor erythropoietin (EPO) and erythropoietin receptors (EPOR) are expressed in the nervous system. Neuronal expression of EPO and EPOR peaks during brain development and is upregulated in the adult brain after injury. Peripherally administered EPO, and at least some of its variants, cross the blood-brain barrier, stimulate neurogenesis, neuronal differentiation, and activate brain neurotrophic, anti-apoptotic, anti-oxidant and anti-inflammatory signaling. These mechanisms underlie their tissue protective effects in nervous system disorders. As the tissue protective functions of EPO can be separated from its stimulatory action on hematopoiesis, novel EPO derivatives and mimetics, such as asialo-EPO and carbamoylated EPO have been developed. While the therapeutic potential of the novel EPO derivatives continues to be characterized in preclinical studies, the experimental findings in support for the use of recombinant human (rh)EPO in human brain disease have already been translated to clinical studies in acute ischemic stroke, chronic schizophrenia, and chronic progressive multiple sclerosis. In this review article, we assess the studies on EPO and, in particular, on its structural or functional variants in experimental models of nervous system disorders, and we provide a short overview of the completed and ongoing clinical studies testing EPO as neuroprotective/neuroregenerative treatment option in neuropsychiatric disease."],["dc.identifier.doi","10.1016/j.nurt.2008.10.041"],["dc.identifier.gro","3150447"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7212"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.subject","Ischemia; cognition; motor function; hematocrit; thrombocytes; safety"],["dc.title","Therapeutic potential of erythropoietin and its structural or functional variants in the nervous system"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","unknown"],["dspace.entity.type","Publication"]]