Reichardt, Sybille D.

[["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","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","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"]]

[["dc.bibliographiccitation.firstpage","65902"],["dc.bibliographiccitation.issue","40"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","65915"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Beschel, L. Milena"],["dc.contributor.author","Leu, Martin"],["dc.contributor.author","Reichardt, Sybille D."],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Schirmer, Markus Anton"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Canis, Martin"],["dc.contributor.author","Wolff, Hendrik Andreas"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.date.accessioned","2018-11-07T10:07:12Z"],["dc.date.available","2018-11-07T10:07:12Z"],["dc.date.issued","2016"],["dc.description.abstract","Treatment of head and neck squamous cell carcinoma (HNSCC) by chemoradiotherapy (CRT) often results in high-grade acute organ toxicity (HGAOT). As these adverse effects impair the patients' quality of life and the feasibility of the planned therapy, we sought to analyze immunological parameters in tumor material and blood samples obtained from 48 HNSCC patients in order to assess the potential to predict the individual acute organ toxicity. T cells in the tumor stroma were enriched in patients developing HGAOT whereas levels of soluble factors in the plasma and gene expression in whole blood did not coincide with the occurrence of acute organ toxicity. In contrast, the frequency and absolute numbers of selected leukocyte subpopulations measured in samples of peripheral blood mononuclear cells (PBMCs) directly before the beginning of CRT were significantly different in patients with HGAOT as compared to those without. When we validated several potential markers including the abundance of T cells in a small prospective study with 16 HNSCC patients, we were able to correctly predict acute organ toxicity in up to 81% of the patients. We conclude that analysis of PBMCs by fluorescence-activated cell sorting (FACS) might be a convenient strategy to identify patients at risk of developing HGAOT caused by CRT, which might allow to adapt the treatment regimen and possibly improve disease outcome."],["dc.description.sponsorship","University Medical Center Gottingen"],["dc.identifier.doi","10.18632/oncotarget.11677"],["dc.identifier.isi","000387281000105"],["dc.identifier.pmid","27589568"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39238"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Impact Journals Llc"],["dc.relation.issn","1949-2553"],["dc.title","T cell abundance in blood predicts acute organ toxicity in chemoradiotherapy for head and neck cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4509"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","The Journal of Immunology"],["dc.bibliographiccitation.lastpage","4516"],["dc.bibliographiccitation.volume","187"],["dc.contributor.author","Tischner, Denise"],["dc.contributor.author","Theiss, Jennifer"],["dc.contributor.author","Karabinskaya, Anna"],["dc.contributor.author","van den Brandt, Jens"],["dc.contributor.author","Reichardt, Sybille D."],["dc.contributor.author","Karow, Ulrike"],["dc.contributor.author","Herold, Marco J."],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Utermoehlen, Olaf"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.date.accessioned","2018-11-07T08:50:13Z"],["dc.date.available","2018-11-07T08:50:13Z"],["dc.date.issued","2011"],["dc.description.abstract","The activity of acid sphingomyelinase (aSMase) was previously reported to be involved in glucocorticoid-induced cell death (GICD) of T lymphocytes. This mechanism in turn is believed to contribute to the therapeutic efficacy of glucocorticoids (GCs) in the treatment of inflammatory diseases. In this study, we reassessed the role of aSMase in GICD by using aSMase knockout mice. The absence of aSMase largely abolished the partial protection that effector memory CD4(+) T cells in wild-type mice possess against GICD. Reduced IL-2 secretion by aSMase-deficient CD4(+) T cells suggested that a lack of this important survival factor might be the cause of these cells' enhanced susceptibility to GICD. Indeed, addition of IL-2 restored the protection against GICD, whereas neutralization of IL-2 abrogated the otherwise protective effect seen in wild-type effector memory CD4(+) T cells. The therapeutic implications of the altered sensitivity of aSMase-deficient T cells to GICD were assessed in models of inflammatory disorders; namely, experimental autoimmune encephalomyelitis and acute graft-versus-host disease. Surprisingly, GC treatment was equally efficient in both models in terms of ameliorating the diseases, regardless of the genotype of the T cells. Thus, our data reveal a hitherto unrecognized contribution of aSMase to the sensitivity of effector memory CD4(+) T cells to GICD and call into question the traditionally attributed importance of GICD of T cells to the treatment of inflammatory diseases by GCs. The Journal of Immunology, 2011, 187: 4509-4516."],["dc.identifier.doi","10.4049/jimmunol.1100911"],["dc.identifier.isi","000296496000017"],["dc.identifier.pmid","21948986"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21648"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Immunologists"],["dc.relation.issn","0022-1767"],["dc.title","Acid Sphingomyelinase Is Required for Protection of Effector Memory T Cells against Glucocorticoid-Induced Cell Death"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","157"],["dc.bibliographiccitation.journal","Journal of Controlled Release"],["dc.bibliographiccitation.lastpage","169"],["dc.bibliographiccitation.volume","245"],["dc.contributor.author","Montes-Cobos, Elena"],["dc.contributor.author","Ring, Sarah"],["dc.contributor.author","Fischer, Henrike J."],["dc.contributor.author","Heck, Joachim G."],["dc.contributor.author","Strauss, Judith"],["dc.contributor.author","Schwaninger, Markus"],["dc.contributor.author","Reichardt, Sybille D."],["dc.contributor.author","Feldmann, Claus"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.date.accessioned","2018-11-07T10:28:25Z"],["dc.date.available","2018-11-07T10:28:25Z"],["dc.date.issued","2017"],["dc.description.abstract","Glucocorticoids (GC) are widely used to treat acute relapses in multiple sclerosis (MS) patients, but their application is accompanied by side effects due to their broad spectrum of action. Here, we report on the therapeutic option to apply GC via inorganic-organic hybrid nanoparticles (IOH-NP) with the composition [ZrO](2+)[(BMP)(0.9)(FMN)(0.1)](2-) (designated BMP-NP with BMP: betamethasone phosphate; FMN: flavinmononucleotide). We found that these BMP-NP have an increased cell type-specificity compared to free GC while retaining full therapeutic efficacy in a mouse model of MS. BMP-NP were preferentially taken up by phagocytic cells and modulated macrophages in vivo more efficiently than T cells. When GC were applied in the form of BMP-NP, treatment of neuroinflammatory disease in mice exclusively depended on the control of macrophage function whereas effects on T cells and brain endothelial cells were dispensable for therapeutic efficacy. Importantly, BMP-NP were not only active in mice but also showed strong activity towards monocytes isolated from healthy human volunteers. We conclude that application of GC via IOH-NP has the potential to improve MS therapy in the future. (C) 2016 Elsevier B.V. All rights reserved."],["dc.description.sponsorship","German Research Foundation (DFG) [RE 1631/15-1, LU 634/9-1]"],["dc.identifier.doi","10.1016/j.jconrel.2016.12.003"],["dc.identifier.isi","000396474500015"],["dc.identifier.pmid","27919626"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43416"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1873-4995"],["dc.relation.issn","0168-3659"],["dc.title","Targeted delivery of glucocorticoids to macrophages in a mouse model of multiple sclerosis using inorganic-organic hybrid nanoparticles"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","68"],["dc.bibliographiccitation.journal","Immunology Letters"],["dc.bibliographiccitation.lastpage","79"],["dc.bibliographiccitation.volume","233"],["dc.contributor.author","Reichardt, Sybille D."],["dc.contributor.author","Lühder, Fred"],["dc.contributor.author","Wiegers, G. Jan"],["dc.contributor.author","Reichardt, Holger M."],["dc.date.accessioned","2021-06-01T09:41:20Z"],["dc.date.available","2021-06-01T09:41:20Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1016/j.imlet.2021.03.010"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84889"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.issn","0165-2478"],["dc.title","A flow cytometric approach to study glucocorticoid receptor expression in immune cell subpopulations of genetically engineered mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3899"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Endocrinology"],["dc.bibliographiccitation.lastpage","3908"],["dc.bibliographiccitation.volume","155"],["dc.contributor.author","Reichardt, Sybille D."],["dc.contributor.author","Weinhage, Toni"],["dc.contributor.author","Rotte, Anand"],["dc.contributor.author","Foeller, Michael"],["dc.contributor.author","Oppermann, Martin"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Tuckermann, Jan P."],["dc.contributor.author","Lang, Florian"],["dc.contributor.author","van den Brandt, Jens"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.date.accessioned","2018-11-07T09:34:44Z"],["dc.date.available","2018-11-07T09:34:44Z"],["dc.date.issued","2014"],["dc.description.abstract","Glucocorticoids (GCs) constitute a highly pleiotropic class of drugs predominantly employed in the treatment of inflammatory diseases. In our search for new mechanisms of action, we identified a hitherto unknown effect of GCs in the gastrointestinal tract. We found that oral administration of dexamethasone (Dex) to mice caused an enlargement of the stomach due to the induction of gastroparesis and that this effect was abolished in GR(dim) mice carrying the A458T mutation in the GC receptor (GR). Gastroparesis was unrelated to the enhanced gastric acid secretion observed after Dex treatment, although both effects were mediated by the same molecular mechanism of the GR. Using conditional GR-knockout mice, we could further rule out that GC effects on enterocytes or myeloid cells were involved in the induction of gastroparesis. In contrast, we found that Dex upregulated arginase 2 (Arg2) in the stomach both at the mRNA and protein level. This suggests that GC treatment leads to a depletion of L-arginine thereby impeding the production of nitric oxide (NO), which is required for gastric motility. We tested this hypothesis by supplementing the drinking water of the mice with exogenous L-arginine to compensate for the presumed shortage of this major substrate of NO synthases. Importantly, this measure completely prevented both the enlargement of the stomach and the induction of gastroparesis after Dex treatment. Our findings raise considerations of combining orally applied GCs with L-arginine to improve tolerability of GC treatment and provide a possible explanation for the antiemetic effects of GCs widely exploited in chemotherapy."],["dc.identifier.doi","10.1210/en.2014-1246"],["dc.identifier.isi","000342345000018"],["dc.identifier.pmid","25057793"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32240"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Endocrine Soc"],["dc.relation.issn","1945-7170"],["dc.relation.issn","0013-7227"],["dc.title","Glucocorticoids Induce Gastroparesis in Mice Through Depletion of L-Arginine"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]