Pölking, Esther

[["dc.bibliographiccitation.firstpage","1514"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Investigative Ophthalmology & Visual Science"],["dc.bibliographiccitation.lastpage","1522"],["dc.bibliographiccitation.volume","45"],["dc.contributor.author","Weishaupt, Jochen H."],["dc.contributor.author","Rohde, Gundula"],["dc.contributor.author","Pölking, Esther"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Bähr, Mathias"],["dc.date.accessioned","2017-09-07T11:43:24Z"],["dc.date.available","2017-09-07T11:43:24Z"],["dc.date.issued","2004"],["dc.description.abstract","Purpose. Erythropoietin (EPO) modulates erythropoiesis by inhibiting apoptosis in erythrocyte progenitors. Recently, EPO has been shown to be protective in experimental models of mechanical trauma, neuroinflammation, cerebral and retinal ischemia, and even in a human stroke trial. However, little is known about EPO signal transduction in vivo and the usefulness of EPO in the prevention of the chronic, purely apoptotic neuronal cell death that contributes to vision loss in glaucoma and the progression of neurodegenerative diseases. Methods. EPO's effects and signaling in the retinal ganglion cell axotomy paradigm were studied by Western blot analysis and immunohistochemistry, receptor expression was characterized in the retina before and after lesion. EPO was injected into the vitreous body to investigate neuroprotection of axotomized rat RGCs. Moreover, EPO's effects were studied in cultures of immunopurified retinal ganglion cells. Signal-transduction pathways transmitting neuroprotective EPO effects in vivo were characterized by the use of specific kinase inhibitors, immunohistochemistry, and Western blot analysis. Results. EPO receptors (EPORs) were expressed on RGC somata and dendrites in vivo. EPOR expression did not significantly change after axotomy. Application of EPO prevented death of neurotrophic-factor-deprived immunopurified rat RGCs in vitro, rescued axotomized RGCs in vivo, and prevented caspase-3 activation. EPO-induced Akt phosphorylation and survival-promoting EPO effects were completely abolished by inhibition of PI-3-kinase. EPO neuroprotection followed a bell-shaped dose-response curve in vitro and in vivo, whereas toxic EPO effects were never observed, even at high concentrations. Conclusions. These data support a potential role for EPO as a therapeutic molecule against predominantly apoptotic neuronal cell death in the context of glaucoma or neurodegenerative diseases and delineate the PI-3-K/Akt pathway as the predominant mediator of EPO neuroprotection in this in vivo paradigm of neuronal cell death."],["dc.identifier.doi","10.1167/iovs.03-1039"],["dc.identifier.gro","3143992"],["dc.identifier.isi","000221084700034"],["dc.identifier.pmid","15111610"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1566"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0146-0404"],["dc.title","Effect of Erythropoietin Axotomy-Induced Apoptosis in Rat Retinal Ganglion Cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","532"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Transactions of the Charles S. Peirce Society"],["dc.bibliographiccitation.volume","54"],["dc.contributor.author","Polke, Christian"],["dc.date.accessioned","2020-12-10T18:43:54Z"],["dc.date.available","2020-12-10T18:43:54Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.2979/trancharpeirsoc.54.4.07"],["dc.identifier.issn","0009-1774"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78261"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Royce and Peirce—Two Models of a personal Divine?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","313"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Pineal Research"],["dc.bibliographiccitation.lastpage","323"],["dc.bibliographiccitation.volume","41"],["dc.contributor.author","Weishaupt, Jochen H."],["dc.contributor.author","Bartels, Claudia"],["dc.contributor.author","Pölking, Esther"],["dc.contributor.author","Dietrich, Jeannine"],["dc.contributor.author","Rohde, Gundula"],["dc.contributor.author","Poeggeler, Burkhard"],["dc.contributor.author","Mertens, Nina"],["dc.contributor.author","Sperling, Swetlana"],["dc.contributor.author","Bohn, Matthias"],["dc.contributor.author","Hüther, Gerald"],["dc.contributor.author","Schneider, Armin"],["dc.contributor.author","Bach, Alfred"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.contributor.author","Hardeland, Rüdiger"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:31Z"],["dc.date.available","2017-09-07T11:46:31Z"],["dc.date.issued","2006"],["dc.description.abstract","Amyotrophic lateral sclerosis (ALS) is the collective term for a fatal motoneuron disease of different etiologies, with oxidative stress as a common molecular denominator of disease progression. Melatonin is an amphiphilic molecule with a unique spectrum of antioxidative effects not conveyed by classical antioxidants. In preparation of a possible future clinical trial, we explored the potential of melatonin as neuroprotective compound and antioxidant in: (1) cultured motoneuronal cells (NSC-34), (2) a genetic mouse model of ALS (SOD1(G93A)-transgenic mice), and (3) a group of 31 patients with sporadic ALS. We found that melatonin attenuates glutamate-induced cell death of cultured motoneurons. In SOD1(G93A)-transgenic mice, high-dose oral melatonin delayed disease progression and extended survival. In a clinical safety study, chronic high-dose (300 mg/day) rectal melatonin was well tolerated during an observation period of up to 2 yr. Importantly, circulating serum protein carbonyls, which provide a surrogate marker for oxidative stress, were elevated in ALS patients, but were normalized to control values by melatonin treatment. This combination of preclinical effectiveness and proven safety in humans suggests that high-dose melatonin is suitable for clinical trials aimed at neuroprotection through antioxidation in ALS."],["dc.identifier.doi","10.1111/j.1600-079X.2006.00377.x"],["dc.identifier.gro","3150526"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7299"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","0742-3098"],["dc.title","Reduced oxidative damage in ALS by high-dose enteral melatonin treatment"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","unknown"],["dspace.entity.type","Publication"]]