Saiepour, Nasrin

[["dc.bibliographiccitation.firstpage","E400"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","E401"],["dc.bibliographiccitation.volume","63"],["dc.contributor.author","Yin, Z."],["dc.contributor.author","Raj, D."],["dc.contributor.author","Saiepour, Nasrin"],["dc.contributor.author","van Dam, D."],["dc.contributor.author","Brouwer, Nieske"],["dc.contributor.author","Eggen, Bart J. L."],["dc.contributor.author","Hanisch, U.-K."],["dc.contributor.author","Hol, E."],["dc.contributor.author","Kamphuis, W."],["dc.contributor.author","Bayer, T."],["dc.contributor.author","De Deyn, P. P."],["dc.contributor.author","Boddeke, Erik"],["dc.date.accessioned","2018-11-07T09:54:20Z"],["dc.date.available","2018-11-07T09:54:20Z"],["dc.date.issued","2015"],["dc.identifier.isi","000356386700671"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36516"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.conference","12th European Meeting on Glial Cell Function in Health and Disease"],["dc.relation.eventlocation","Bilbao, SPAIN"],["dc.relation.issn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.title","beta-amyloid plaque-associated microglia priming in transgenic mouse models of Alzheimer's disease"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.volume","63"],["dc.contributor.author","Saiepour, Nasrin"],["dc.contributor.author","Bayer, Thomas A."],["dc.contributor.author","Boddeke, Hendrikus W. G. M."],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.date.accessioned","2018-11-07T09:54:19Z"],["dc.date.available","2018-11-07T09:54:19Z"],["dc.date.issued","2015"],["dc.format.extent","E350"],["dc.identifier.isi","000356386700594"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36512"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.conference","12th European Meeting on Glial Cell Function in Health and Disease"],["dc.relation.eventlocation","Bilbao, SPAIN"],["dc.relation.issn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.title","Functional properties of microglia in mouse models of Alzheimer's disease"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","205"],["dc.bibliographiccitation.journal","Brain Behavior and Immunity"],["dc.bibliographiccitation.lastpage","221"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Schaafsma, W."],["dc.contributor.author","Zhang, X."],["dc.contributor.author","van Zomeren, K. C."],["dc.contributor.author","Jacobs, S."],["dc.contributor.author","Georgieva, Petya B."],["dc.contributor.author","Wolf, S. A."],["dc.contributor.author","Kettenmann, Helmut"],["dc.contributor.author","Janova, Hana"],["dc.contributor.author","Saiepour, Nasrin"],["dc.contributor.author","Hanisch, U.-K."],["dc.contributor.author","Meerlo, Peter"],["dc.contributor.author","van den Elsen, Peter J."],["dc.contributor.author","Brouwer, Nieske"],["dc.contributor.author","Boddeke, Hendrikus W. G. M."],["dc.contributor.author","Eggen, Bart J. L."],["dc.date.accessioned","2018-11-07T09:53:59Z"],["dc.date.available","2018-11-07T09:53:59Z"],["dc.date.issued","2015"],["dc.description.abstract","Microglia, the innate immune cells of the central nervous system (CNS), react to endotoxins like bacterial lipopolysaccharides (LPS) with a pronounced inflammatory response. To avoid excess damage to the CNS, the microglia inflammatory response needs to be tightly regulated. Here we report that a single LPS challenge results in a prolonged blunted pro-inflammatory response to a subsequent LPS stimulation, both in primary microglia cultures (100 ng/ml) and in vivo after intraperitoneal (0.25 and 1 mg/kg) or intracere-broventricular (5 mu g) LPS administration. Chromatin immunoprecipitation (ChIP) experiments with primary microglia and microglia acutely isolated from mice showed that LPS preconditioning was accompanied by a reduction in active histone modifications AcH3 and H3K4me3 in the promoters of the IL-10 and TNF-alpha genes. Furthermore, LPS preconditioning resulted in an increase in the amount of repressive histone modification H3K9me2 in the IL-1 beta promoter. ChIP and knock-down experiments showed that NF-kappa B subunit RelB was bound to the IL-1 beta promoter in preconditioned microglia and that RelB is required for the attenuated LPS response. In addition to a suppressed pro-inflammatory response, preconditioned primary microglia displayed enhanced phagocytic activity, increased outward potassium currents and nitric oxide production in response to a second LPS challenge. In vivo, a single i.p. LPS injection resulted in reduced performance in a spatial learning task 4 weeks later, indicating that a single inflammatory episode affected memory formation in these mice. Summarizing, we show that LPS-preconditioned microglia acquire an epigenetically regulated, immune-suppressed phenotype, possibly to prevent excessive damage to the central nervous system in case of recurrent (peripheral) inflammation. (C) 2015 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.bbi.2015.03.013"],["dc.identifier.isi","000358460700023"],["dc.identifier.pmid","25843371"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36442"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","1090-2139"],["dc.relation.issn","0889-1591"],["dc.title","Long-lasting pro-inflammatory suppression of microglia by LPS-preconditioning is mediated by RelB-dependent epigenetic silencing"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","115"],["dc.bibliographiccitation.journal","Neurobiology of Aging"],["dc.bibliographiccitation.lastpage","122"],["dc.bibliographiccitation.volume","55"],["dc.contributor.author","Yin, Zhuoran"],["dc.contributor.author","Raj, Divya"],["dc.contributor.author","Saiepour, Nasrin"],["dc.contributor.author","Van Dam, Debby"],["dc.contributor.author","Brouwer, Nieske"],["dc.contributor.author","Holtman, Inge R."],["dc.contributor.author","Eggen, Bart J.L."],["dc.contributor.author","Möller, Thomas"],["dc.contributor.author","Tamm, Joseph A."],["dc.contributor.author","Abdourahman, Aicha"],["dc.contributor.author","Hol, Elly M."],["dc.contributor.author","Kamphuis, Willem"],["dc.contributor.author","Bayer, Thomas A."],["dc.contributor.author","De Deyn, Peter P."],["dc.contributor.author","Boddeke, Erik"],["dc.date.accessioned","2020-12-10T15:20:27Z"],["dc.date.available","2020-12-10T15:20:27Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1016/j.neurobiolaging.2017.03.021"],["dc.identifier.issn","0197-4580"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72674"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Immune hyperreactivity of Aβ plaque-associated microglia in Alzheimer's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","911"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","922"],["dc.bibliographiccitation.volume","64"],["dc.contributor.author","Albrecht, Anne"],["dc.contributor.author","Ivens, Sebastian"],["dc.contributor.author","Papageorgiou, Ismini E."],["dc.contributor.author","Caliskan, Gursel"],["dc.contributor.author","Saiepour, Nasrin"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Richter-Levin, Gal"],["dc.contributor.author","Heinemann, Uwe"],["dc.contributor.author","Stork, Oliver"],["dc.date.accessioned","2018-11-07T10:14:00Z"],["dc.date.available","2018-11-07T10:14:00Z"],["dc.date.issued","2016"],["dc.description.abstract","Childhood trauma is a well-described risk factor for the development of stress-related psychopathology such as posttraumatic stress disorder or depression later in life. Childhood adversity can be modeled in rodents by juvenile stress (JS) protocols, resulting in impaired coping with stressful challenges in adulthood. In the current study, we investigated the long-lasting impact of JS on the expression of molecular factors for glutamate and gamma-aminobutyric acid (GABA) uptake and turnover in sublayers of the dentate gyrus (DG) using laser microdissection and quantitative real-time polymerase chain reaction. We observed reduced mRNA expression levels after JS for factors mediating astrocytic glutamate and GABA uptake and degradation. These alterations were prominently observed in the dorsal but not ventral DG granule cell layer, indicating a lasting change in astrocytic GABA and glutamate metabolism that may affect dorsal DG network activity. Indeed, we observed increased inhibition and a lack of facilitation in response to paired-pulse stimulation at short interstimulus intervals in the dorsal DG after JS, while no alterations were evident in basal synaptic transmission or forms of long-term plasticity. The shift in paired-pulse response was mimicked by pharmacologically blocking the astrocytic GABA transporter GAT-3 in naive animals. Accordingly, reduced expression levels of GAT-3 were confirmed at the protein level in the dorsal granule cell layer of rats stressed in juvenility. Together, these data demonstrate a lasting shift in the excitatory/inhibitory balance of dorsal DG network activity by JS that appears to be mediated by decreased GABA uptake into astrocytes."],["dc.identifier.doi","10.1002/glia.22970"],["dc.identifier.isi","000374326600003"],["dc.identifier.pmid","26875694"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40544"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.title","Shifts in Excitatory/Inhibitory Balance by Juvenile Stress: A Role for Neuron-Astrocyte Interaction in the Dentate Gyrus"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","635"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","649"],["dc.bibliographiccitation.volume","64"],["dc.contributor.author","Janova, Hana"],["dc.contributor.author","Böttcher, Chotima"],["dc.contributor.author","Holtman, Inge R."],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Rossum, Denise van"],["dc.contributor.author","Götz, Alexander"],["dc.contributor.author","Ernst, Anne-Sophie"],["dc.contributor.author","Fritsche, Christin"],["dc.contributor.author","Gertig, Ulla"],["dc.contributor.author","Saiepour, Nasrin"],["dc.contributor.author","Gronke, Konrad"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Rolfes, Simone"],["dc.contributor.author","Weinstein, Jonathan"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Kopatz, Jens"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Salinas-Riester, Gabriela"],["dc.contributor.author","Weber, Martin S."],["dc.contributor.author","Prinz, Marco"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Eggen, Bart J. L."],["dc.contributor.author","Boddeke, Hendrikus W. G. M."],["dc.contributor.author","Priller, Josef"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.date.accessioned","2017-09-07T11:45:34Z"],["dc.date.available","2017-09-07T11:45:34Z"],["dc.date.issued","2016"],["dc.description.abstract","Microglia, innate immune cells of the CNS, sense infection and damage through overlapping receptor sets. Toll-like receptor (TLR) 4 recognizes bacterial lipopolysaccharide (LPS) and multiple injury-associated factors. We show that its co-receptor CD14 serves three non-redundant functions in microglia. First, it confers an up to 100-fold higher LPS sensitivity compared to peripheral macrophages to enable efficient proinflammatory cytokine induction. Second, CD14 prevents excessive responses to massive LPS challenges via an interferon β-mediated feedback. Third, CD14 is mandatory for microglial reactions to tissue damage-associated signals. In mice, these functions are essential for balanced CNS responses to bacterial infection, traumatic and ischemic injuries, since CD14 deficiency causes either hypo- or hyperinflammation, insufficient or exaggerated immune cell recruitment or worsened stroke outcomes. While CD14 orchestrates functions of TLR4 and related immune receptors, it is itself regulated by TLR and non-TLR systems to thereby fine-tune microglial damage-sensing capacity upon infectious and non-infectious CNS challenges."],["dc.identifier.doi","10.1002/glia.22955"],["dc.identifier.gro","3150405"],["dc.identifier.pmid","26683584"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7166"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","0894-1491"],["dc.title","CD14 is a key organizer of microglial responses to CNS infection and injury"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1176"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","1185"],["dc.bibliographiccitation.volume","65"],["dc.contributor.author","Doering, Christin"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Gertig, Ulla"],["dc.contributor.author","van Rossum, Denise"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Saiepour, Nasrin"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.contributor.author","Janova, Hana"],["dc.date.accessioned","2018-11-07T10:22:27Z"],["dc.date.available","2018-11-07T10:22:27Z"],["dc.date.issued","2017"],["dc.description.abstract","Microglia as principle innate immune cells of the central nervous system (CNS) are the first line of defense against invading pathogens. They are capable of sensing infections through diverse receptors, such as Toll-like receptor 4 (TLR4). This receptor is best known for its ability to recognize bacterial lipopolysaccharide (LPS), a causative agent of gram-negative sepsis and septic shock. A putative, naturally occurring antagonist of TLR4 derives from the photosynthetic bacterium Rhodobacter sphaeroides. However, the antagonistic potential of R. sphaeroides LPS (Rs-LPS) is no universal feature, since several studies suggested agonistic rather than antagonistic actions of this molecule depending on the investigated mammalian species. Here we show the agonistic versus antagonistic potential of Rs-LPS in primary mouse microglia. We demonstrate that Rs-LPS efficiently induces the release of cytokines and chemokines, which depends on TLR4, MyD88, and TRIF, but not CD14. Furthermore, Rs-LPS is able to regulate the phagocytic capacity of microglia as agonist, while it antagonizes Re-LPS-induced MHC I expression. Finally, to our knowledge, we are the first to provide in vivo evidence for an agonistic potential of Rs-LPS, as it efficiently triggers the recruitment of peripheral immune cells to the endotoxin-challenged CNS. Together, our results argue for a versatile and complex organization of the microglial TLR4 system, which specifically translates exogenous signals into cellular functions. Importantly, as demonstrated here for microglia, the antagonistic potential of Rs-LPS needs to be considered with caution, as reactions to Rs-LPS not only differ by cell type, but even by function within one cell type."],["dc.description.sponsorship","German Research Council (DFG) [SFB/TRR43, FOR1336]"],["dc.identifier.doi","10.1002/glia.23151"],["dc.identifier.isi","000401345400011"],["dc.identifier.pmid","28471051"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42277"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Wiley"],["dc.relation.issn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.title","A presumed antagonistic LPS identifies distinct functional organization of TLR4 in mouse microglia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","204"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Molecular Ecology Resources"],["dc.bibliographiccitation.lastpage","215"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Gogarten, Jan F."],["dc.contributor.author","Calvignac‐Spencer, Sébastien"],["dc.contributor.author","Nunn, Charles L."],["dc.contributor.author","Ulrich, Markus"],["dc.contributor.author","Saiepour, Nasrin"],["dc.contributor.author","Nielsen, Henrik Vedel"],["dc.contributor.author","Deschner, Tobias"],["dc.contributor.author","Fichtel, Claudia"],["dc.contributor.author","Kappeler, Peter M."],["dc.contributor.author","Knauf, Sascha"],["dc.contributor.author","Müller‐Klein, Nadine"],["dc.contributor.author","Ostner, Julia"],["dc.contributor.author","Robbins, Martha M."],["dc.contributor.author","Sangmaneedet, Somboon"],["dc.contributor.author","Schülke, Oliver"],["dc.contributor.author","Surbeck, Martin"],["dc.contributor.author","Wittig, Roman M."],["dc.contributor.author","Sliwa, Alexander"],["dc.contributor.author","Strube, Christina"],["dc.contributor.author","Leendertz, Fabian H."],["dc.contributor.author","Roos, Christian"],["dc.contributor.author","Noll, Angela"],["dc.date.accessioned","2021-04-14T08:27:47Z"],["dc.date.available","2021-04-14T08:27:47Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1111/1755-0998.13101"],["dc.identifier.eissn","1755-0998"],["dc.identifier.issn","1755-098X"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82401"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1755-0998"],["dc.relation.issn","1755-098X"],["dc.title","Metabarcoding of eukaryotic parasite communities describes diverse parasite assemblages spanning the primate phylogeny"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]