Reichardt, Sybille D.

[["dc.bibliographiccitation.firstpage","1220"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","European Journal of Immunology"],["dc.bibliographiccitation.lastpage","1233"],["dc.bibliographiccitation.volume","50"],["dc.contributor.author","Kaiser, Tina K."],["dc.contributor.author","Li, Hu"],["dc.contributor.author","Roßmann, Laura"],["dc.contributor.author","Reichardt, Sybille D."],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Feldmann, Claus"],["dc.contributor.author","Reichardt, Holger M."],["dc.date.accessioned","2021-04-14T08:27:15Z"],["dc.date.available","2021-04-14T08:27:15Z"],["dc.date.issued","2020"],["dc.description.abstract","Abstract Glucocorticoids (GCs) are widely used to treat acute graft‐versus‐host disease (aGvHD) due to their immunosuppressive activity, but they also reduce the beneficial graft‐versus‐leukemia (GvL) effect of the allogeneic T cells contained in the graft. Here, we tested whether aGvHD therapy could be improved by delivering GCs with the help of inorganic–organic hybrid nanoparticles (IOH‐NPs) that preferentially target myeloid cells. IOH‐NPs containing the GC betamethasone (BMP‐NPs) efficiently reduced morbidity, mortality, and tissue damage in a totally MHC mismatched mouse model of aGvHD. Therapeutic activity was lost in mice lacking the GC receptor (GR) in myeloid cells, confirming the cell type specificity of our approach. BMP‐NPs had no relevant systemic activity but suppressed cytokine and chemokine gene expression locally in the small intestine, which presumably explains their mode of action. Most importantly, BMP‐NPs delayed the development of an adoptively transferred B cell lymphoma better than the free drug, although the overall incidence was unaffected. Our findings thus suggest that employing IOH‐NPs could diminish the risk of relapse associated with GC therapy of aGvHD patients while still allowing to efficiently ameliorate the disease."],["dc.description.abstract","Clinical symptoms and histological hallmarks of acute graft‐versus‐host disease in mice are ameliorated by glucocorticoids when specifically delivered to macrophages with the help of nanoparticles. In addition, this therapeutic intervention improves the graft‐versus‐leukemia effect compared to the free drug, and thus presumably reduces the risk of relapse. image"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft http://dx.doi.org/10.13039/501100001659"],["dc.identifier.doi","10.1002/eji.201948464"],["dc.identifier.eissn","1521-4141"],["dc.identifier.issn","0014-2980"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82221"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1521-4141"],["dc.relation.issn","0014-2980"],["dc.rights","This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited."],["dc.title","Glucocorticoids delivered by inorganic–organic hybrid nanoparticles mitigate acute graft‐versus‐host disease and sustain graft‐versus‐leukemia activity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1505"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Cellular and Molecular Gastroenterology and Hepatology"],["dc.bibliographiccitation.lastpage","1518"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Muzzi, Chiara"],["dc.contributor.author","Watanabe, Norika"],["dc.contributor.author","Twomey, Eric"],["dc.contributor.author","Meers, Garrit K."],["dc.contributor.author","Reichardt, Holger M."],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Reichardt, Sybille D."],["dc.date.accessioned","2021-06-01T09:41:22Z"],["dc.date.available","2021-06-01T09:41:22Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1016/j.jcmgh.2020.12.006"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17779"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84897"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2352-345X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","The Glucocorticoid Receptor in Intestinal Epithelial Cells Alleviates Colitis and Associated Colorectal Cancer in Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","E1"],["dc.bibliographiccitation.issue","7552"],["dc.bibliographiccitation.journal","Nature"],["dc.bibliographiccitation.lastpage","U379"],["dc.bibliographiccitation.volume","521"],["dc.contributor.author","Wang, Jieqi"],["dc.contributor.author","Wegener, Jan Eike"],["dc.contributor.author","Huang, Teng-Wei"],["dc.contributor.author","Sripathy, Smitha"],["dc.contributor.author","Jesus-Cortes, Hector de"],["dc.contributor.author","Xu, Pin"],["dc.contributor.author","Tran, Stephanie"],["dc.contributor.author","Knobbe, Whitney"],["dc.contributor.author","Leko, Vid"],["dc.contributor.author","Britt, Jeremiah"],["dc.contributor.author","Starwalt, Ruth"],["dc.contributor.author","McDaniel, Latisha"],["dc.contributor.author","Ward, Chris S."],["dc.contributor.author","Parra, Diana"],["dc.contributor.author","Newcomb, Benjamin"],["dc.contributor.author","Lao, Uyen"],["dc.contributor.author","Nourigat, Cynthia"],["dc.contributor.author","Flowers, David A."],["dc.contributor.author","Cullen, Sean"],["dc.contributor.author","Jorstad, Nikolas L."],["dc.contributor.author","Yang, Yue"],["dc.contributor.author","Glaskova, Lena"],["dc.contributor.author","Vigneau, Sebastian"],["dc.contributor.author","Kozlitina, Julia"],["dc.contributor.author","Yetman, Michael J."],["dc.contributor.author","Jankowsky, Joanna L."],["dc.contributor.author","Reichardt, Sybille D."],["dc.contributor.author","Reichardt, Holger M."],["dc.contributor.author","Gärtner, Jutta"],["dc.contributor.author","Bartolomei, Marisa S."],["dc.contributor.author","Fang, Min"],["dc.contributor.author","Loeb, Keith"],["dc.contributor.author","Keene, C. Dirk"],["dc.contributor.author","Bernstein, Irwin"],["dc.contributor.author","Goodell, Margaret"],["dc.contributor.author","Brat, Daniel J."],["dc.contributor.author","Huppke, Peter"],["dc.contributor.author","Neul, Jeffrey L."],["dc.contributor.author","Bedalov, Antonio"],["dc.contributor.author","Pieper, Andrew A."],["dc.date.accessioned","2017-09-07T11:44:23Z"],["dc.date.available","2017-09-07T11:44:23Z"],["dc.date.issued","2015"],["dc.identifier.doi","10.1038/nature14444"],["dc.identifier.gro","3141899"],["dc.identifier.isi","000354816500014"],["dc.identifier.pmid","25993969"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2311"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1476-4687"],["dc.relation.issn","0028-0836"],["dc.title","Wild-type microglia do not reverse pathology in mouse models of Rett syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2921"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Cells"],["dc.bibliographiccitation.volume","10"],["dc.contributor.affiliation","Reichardt, Sybille D.; 1Institute for Cellular and Molecular Immunology, University Medical Center Göttingen, 37073 Göttingen, Germany; sybille.reichardt@med.uni-goettingen.de (S.D.R.); agathe.amouret@med.uni-goettingen.de (A.A.); chiara.muzzi@med.uni-goettingen.de (C.M.)"],["dc.contributor.affiliation","Amouret, Agathe; 1Institute for Cellular and Molecular Immunology, University Medical Center Göttingen, 37073 Göttingen, Germany; sybille.reichardt@med.uni-goettingen.de (S.D.R.); agathe.amouret@med.uni-goettingen.de (A.A.); chiara.muzzi@med.uni-goettingen.de (C.M.)"],["dc.contributor.affiliation","Muzzi, Chiara; 1Institute for Cellular and Molecular Immunology, University Medical Center Göttingen, 37073 Göttingen, Germany; sybille.reichardt@med.uni-goettingen.de (S.D.R.); agathe.amouret@med.uni-goettingen.de (A.A.); chiara.muzzi@med.uni-goettingen.de (C.M.)"],["dc.contributor.affiliation","Vettorazzi, Sabine; 2Institute of Comparative Molecular Endocrinology, Ulm University, 89081 Ulm, Germany; sabine.vettorazzi@uni-ulm.de (S.V.); jan.tuckermann@uni-ulm.de (J.P.T.)"],["dc.contributor.affiliation","Tuckermann, Jan P.; 2Institute of Comparative Molecular Endocrinology, Ulm University, 89081 Ulm, Germany; sabine.vettorazzi@uni-ulm.de (S.V.); jan.tuckermann@uni-ulm.de (J.P.T.)"],["dc.contributor.affiliation","Lühder, Fred; 3Institute for Neuroimmunology and Multiple Sclerosis Research, University Medical Center Göttingen, 37075 Göttingen, Germany; fred.luehder@med.uni-goettingen.de"],["dc.contributor.affiliation","Reichardt, Holger M.; 1Institute for Cellular and Molecular Immunology, University Medical Center Göttingen, 37073 Göttingen, Germany; sybille.reichardt@med.uni-goettingen.de (S.D.R.); agathe.amouret@med.uni-goettingen.de (A.A.); chiara.muzzi@med.uni-goettingen.de (C.M.)"],["dc.contributor.author","Reichardt, Sybille D."],["dc.contributor.author","Amouret, Agathe"],["dc.contributor.author","Muzzi, Chiara"],["dc.contributor.author","Vettorazzi, Sabine"],["dc.contributor.author","Tuckermann, Jan P."],["dc.contributor.author","Lühder, Fred"],["dc.contributor.author","Reichardt, Holger M."],["dc.date.accessioned","2022-01-11T14:07:51Z"],["dc.date.available","2022-01-11T14:07:51Z"],["dc.date.issued","2021"],["dc.date.updated","2022-02-09T13:20:27Z"],["dc.description.abstract","For more than 70 years, glucocorticoids (GCs) have been a powerful and affordable treatment option for inflammatory diseases. However, their benefits do not come without a cost, since GCs also cause side effects. Therefore, strong efforts are being made to improve their therapeutic index. In this review, we illustrate the mechanisms and target cells of GCs in the pathogenesis and treatment of some of the most frequent inflammatory disorders affecting the central nervous system, the gastrointestinal tract, the lung, and the joints, as well as graft-versus-host disease, which often develops after hematopoietic stem cell transplantation. In addition, an overview is provided of novel approaches aimed at improving GC therapy based on chemical modifications or GC delivery using nanoformulations. GCs remain a topic of highly active scientific research despite being one of the oldest class of drugs in medical use."],["dc.description.abstract","For more than 70 years, glucocorticoids (GCs) have been a powerful and affordable treatment option for inflammatory diseases. However, their benefits do not come without a cost, since GCs also cause side effects. Therefore, strong efforts are being made to improve their therapeutic index. In this review, we illustrate the mechanisms and target cells of GCs in the pathogenesis and treatment of some of the most frequent inflammatory disorders affecting the central nervous system, the gastrointestinal tract, the lung, and the joints, as well as graft-versus-host disease, which often develops after hematopoietic stem cell transplantation. In addition, an overview is provided of novel approaches aimed at improving GC therapy based on chemical modifications or GC delivery using nanoformulations. GCs remain a topic of highly active scientific research despite being one of the oldest class of drugs in medical use."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.3390/cells10112921"],["dc.identifier.eissn","2073-4409"],["dc.identifier.pii","cells10112921"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/97878"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-507"],["dc.relation.eissn","2073-4409"],["dc.relation.orgunit","Institut für Zelluläre und Molekulare Immunologie"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","The Role of Glucocorticoids in Inflammatory Diseases"],["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","174"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neuroendocrinology"],["dc.bibliographiccitation.lastpage","182"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Schweingruber, Nils"],["dc.contributor.author","Reichardt, Sybille D."],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.date.accessioned","2018-11-07T09:15:58Z"],["dc.date.available","2018-11-07T09:15:58Z"],["dc.date.issued","2012"],["dc.description.abstract","Glucocorticoids (GCs) are widely used to treat inflammatory diseases such as multiple sclerosis (MS). They predominantly act through the GC receptor, a member of the nuclear receptor superfamily that controls transcription by several different mechanisms. Owing to its ubiquitous expression, there are a variety of cell types that could serve as GC targets in the pathogenesis and treatment of MS. This brings about a great diversity of mechanisms potentially involved in the modulation of neuroinflammation by GCs, including the induction of apoptosis, repression of pro-inflammatory mediators and the expansion of myeloid-derived suppressor cells. Nevertheless, it is not well understood which of these mechanisms are essential for therapeutic efficacy. In this review, we summarise findings made concerning the actions of GCs in MS and its animal model experimental autoimmune encephalomyelitis, and also elucidate current concepts and developments that pertain to this clinically highly relevant treatment regimen."],["dc.identifier.doi","10.1111/j.1365-2826.2011.02161.x"],["dc.identifier.isi","000298601800016"],["dc.identifier.pmid","21615563"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27832"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0953-8194"],["dc.title","Mechanisms of Glucocorticoids in the Control of Neuroinflammation"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","15437"],["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","15450"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Baake, Tina"],["dc.contributor.author","Jörß, Katharina"],["dc.contributor.author","Suennemann, Jennifer"],["dc.contributor.author","Roßmann, Laura"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Tuckermann, Jan P."],["dc.contributor.author","Reichardt, Holger M."],["dc.contributor.author","Fischer, Henrike J."],["dc.contributor.author","Reichardt, Sybille D."],["dc.date.accessioned","2019-07-09T11:45:14Z"],["dc.date.available","2019-07-09T11:45:14Z"],["dc.date.issued","2018"],["dc.description.abstract","Graft-versus-host disease (GvHD) is a life-threatening complication of hematopoietic stem cell transplantation (HSCT), which is caused by allogeneic T cells recognizing molecules of the recipient as foreign. Endogenous glucocorticoids (GC) released from the adrenal gland are crucial in regulating such inflammatory diseases. Here we demonstrate that genetically engineered mice, that are largely unresponsive to GC, suffer from aggravated clinical symptoms and increased mortality after HSCT, effects that could be tempered by neutralization of IL-6. Interestingly, selective ablation of the GC receptor (GR) in recipient myeloid cells resulted in fulminant disease as well. While histopathological analysis of the jejunum failed to reveal any differences between sick mice of both genotypes, systemic IL-6 and TNFα secretion was strongly increased in transplanted mice lacking the GR in myeloid cells briefly before the majority of them succumbed to the disease. Collectively, our findings reveal an important role of the GR in recipient cells in limiting the cytokine storm caused by GvHD induction."],["dc.identifier.doi","10.18632/oncotarget.24602"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15071"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59189"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.subject.ddc","610"],["dc.title","The glucocorticoid receptor in recipient cells keeps cytokine secretion in acute graft-versus-host disease at bay"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0190846"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","PLOS ONE"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Meers, Garrit K."],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Reichardt, Holger M."],["dc.contributor.author","Lühder, Fred"],["dc.contributor.author","Reichardt, Sybille D."],["dc.date.accessioned","2019-07-09T11:45:08Z"],["dc.date.available","2019-07-09T11:45:08Z"],["dc.date.issued","2018"],["dc.description.abstract","Inflammatory bowel disease (IBD) is a highly prevalent intestinal disorder for which no cure exists. Currently, the standard first-line treatment of IBD consists of systemic glucocorticoid (GC) application, even though therapy can be complicated by unresponsiveness or adverse effects. In view of the importance of macrophages and neutrophils for the pathogenesis of IBD we set out to define the relevance of these cell types as targets of GC using the mouse model of DSS-induced colitis. We found that the disease did not resolve in GRlysM mice lacking the GC receptor (GR) in myeloid cells after removal of the chemical insult. While clinical symptoms and tissue damage in the colon ameliorated again in GRflox mice, the disease further aggravated in GRlysM littermates. The observed difference coincided with an increased abundance of macrophages in inflammatory infiltrates in the colon of mutant mice whereas neutrophil and T cell numbers were similar. Concomitantly, systemic IL-6 secretion and mRNA levels of pro-inflammatory cytokines in the colon were elevated in GRlysM mice and gene expression of scavenger receptors and IL-10 was diminished. Taken together, our results reveal an important role of myeloid cells as targets of GC in DSS-induced colitis and probably in IBD in humans as well."],["dc.identifier.doi","10.1371/journal.pone.0190846"],["dc.identifier.pmid","29324769"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15039"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59164"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Colitis"],["dc.subject.mesh","Colon"],["dc.subject.mesh","Dextran Sulfate"],["dc.subject.mesh","Disease Models, Animal"],["dc.subject.mesh","Interleukin-10"],["dc.subject.mesh","Interleukin-6"],["dc.subject.mesh","Intestinal Mucosa"],["dc.subject.mesh","Mice, Inbred C57BL"],["dc.subject.mesh","Mice, Transgenic"],["dc.subject.mesh","Myeloid Cells"],["dc.subject.mesh","RNA, Messenger"],["dc.subject.mesh","Receptors, Glucocorticoid"],["dc.title","Impaired resolution of DSS-induced colitis in mice lacking the glucocorticoid receptor in myeloid cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","646"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The Journal of Pathology"],["dc.bibliographiccitation.lastpage","655"],["dc.bibliographiccitation.volume","235"],["dc.contributor.author","Theiss-Suennemann, Jennifer"],["dc.contributor.author","Joerss, Katharina"],["dc.contributor.author","Messmann, Joanna J."],["dc.contributor.author","Reichardt, Sybille D."],["dc.contributor.author","Montes-Cobos, Elena"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Tuckermann, Jan P."],["dc.contributor.author","Wolff, Hendrik Andreas"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Groene, Hermann-Josef"],["dc.contributor.author","Strauss, Gudrun"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.date.accessioned","2018-11-07T10:00:41Z"],["dc.date.available","2018-11-07T10:00:41Z"],["dc.date.issued","2015"],["dc.description.abstract","Glucocorticoids (GCs) are released from the adrenal gland during inflammation and help to keep immune responses at bay. Owing to their potent anti-inflammatory activity, GCs also play a key role in controlling acute graft-versus-host disease (aGvHD). Here we demonstrate that mice lacking the glucocorticoid receptor (GR) in T cells develop fulminant disease after allogeneic bone marrow transplantation. In a fully MHC-mismatched model, transfer of GR-deficient T cells resulted in severe aGvHD symptoms and strongly decreased survival times. Histopathological features were aggravated and infiltration of CD8(+) T cells into the jejunum was increased when the GR was not expressed. Furthermore, serum levels of IL-2, IFN, and IL-17 were elevated and the cytotoxicity of CD8(+) T cells was enhanced after transfer of GR-deficient T cells. Short-term treatment with dexamethasone reduced cytokine secretion but neither impacted disease severity nor the CTLs' cytolytic capacity. Importantly, in an aGvHD model in which disease development exclusively depends on the presence of CD8(+) T cells in the transplant, transfer of GR-deficient T cells aggravated clinical symptoms and reduced survival times as well. Taken together, our findings highlight that suppression of CD8(+) T-cell function is a crucial mechanism in the control of aGvHD by endogenous GCs. Copyright (c) 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd."],["dc.identifier.doi","10.1002/path.4475"],["dc.identifier.isi","000349677700011"],["dc.identifier.pmid","25358639"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37861"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1096-9896"],["dc.relation.issn","0022-3417"],["dc.title","Glucocorticoids attenuate acute graft-versus-host disease by suppressing the cytotoxic capacity of CD8(+) T cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","105485"],["dc.bibliographiccitation.journal","The Journal of Steroid Biochemistry and Molecular Biology"],["dc.bibliographiccitation.volume","195"],["dc.contributor.author","Li, Hu"],["dc.contributor.author","Kaiser, Tina K."],["dc.contributor.author","Borschiwer, Marina"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Reichardt, Sybille D."],["dc.contributor.author","Lühder, Fred"],["dc.contributor.author","Walter, Lutz"],["dc.contributor.author","Dressel, Ralf"],["dc.contributor.author","Meijsing, Sebastiaan H."],["dc.contributor.author","Reichardt, Holger M."],["dc.date.accessioned","2020-12-10T14:25:26Z"],["dc.date.available","2020-12-10T14:25:26Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1016/j.jsbmb.2019.105485"],["dc.identifier.issn","0960-0760"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72552"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Glucocorticoid resistance of allogeneic T cells alters the gene expression profile in the inflamed small intestine of mice suffering from acute graft-versus-host disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1783"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Endocrinology"],["dc.bibliographiccitation.lastpage","1794"],["dc.bibliographiccitation.volume","153"],["dc.contributor.author","Reichardt, Sybille D."],["dc.contributor.author","Foeller, Michael"],["dc.contributor.author","Rexhepaj, Rexhep"],["dc.contributor.author","Pathare, Ganesh"],["dc.contributor.author","Minnich, Kerstin"],["dc.contributor.author","Tuckermann, Jan P."],["dc.contributor.author","Lang, Florian"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.date.accessioned","2018-11-07T09:11:45Z"],["dc.date.available","2018-11-07T09:11:45Z"],["dc.date.issued","2012"],["dc.description.abstract","Glucocorticoid (GC) treatment of inflammatory disorders, such as inflammatory bowel disease, causes deranged metabolism, in part by enhanced intestinal resorption of glucose. However, the underlying molecular mechanism is poorly understood. Hence, we investigated transcriptional control of genes reported to be involved in glucose uptake in the small intestine after GC treatment and determined effects of GC on electrogenic glucose transport from transepithelial currents. GR(villinCre) mice lacking the GC receptor (GR) in enterocytes served to identify the target cell of GC treatment and the requirement of the GR itself; GR(dim) mice impaired in dimerization and DNA binding of the GR were used to determine the underlying molecular mechanism. Our findings revealed that oral administration of dexamethasone to wild-type mice for 3 d increased mRNA expression of serum- and GC-inducible kinase 1, sodium-coupled glucose transporter 1, and Na+/H+ exchanger 3, as well as electrogenic glucose transport in the small intestine. In contrast, GRvillinCre mice did not respond to GC treatment, neither with regard to gene activation nor to glucose transport. GRdim mice were also refractory to GC, because dexamethasone treatment failed to increase both, gene expression and electrogenic glucose transport. In addition, the rise in blood glucose levels normally observed after GC administration was attenuated in both mutant mouse strains. We conclude that enhanced glucose transport in vivo primarily depends on gene regulation by the dimerized GR in enterocytes, and that this mechanism contributes to GC-induced hyperglycemia. (Endocrinology 153: 1783-1794, 2012)"],["dc.identifier.doi","10.1210/en.2011-1747"],["dc.identifier.isi","000302169800027"],["dc.identifier.pmid","22294744"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26791"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Endocrine Soc"],["dc.relation.issn","0013-7227"],["dc.title","Glucocorticoids Enhance Intestinal Glucose Uptake Via the Dimerized Glucocorticoid Receptor in Enterocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]