Ramadori, Giuliano

[["dc.bibliographiccitation.firstpage","388"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Cellular Physiology"],["dc.bibliographiccitation.lastpage","398"],["dc.bibliographiccitation.volume","199"],["dc.contributor.author","Novosyadlyy, R."],["dc.contributor.author","Tron, Kyrylo"],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Scharf, Jens-Gerd"],["dc.date.accessioned","2018-11-07T10:48:32Z"],["dc.date.available","2018-11-07T10:48:32Z"],["dc.date.issued","2004"],["dc.description.abstract","Apart from hepatic stellate cells (HSC), liver myofibroblasts (MF) represent a second mesenchymal cell population involved in hepatic fibrogenesis. The IGF system including the insulin-like growth factors I and II (IGF-I, -II), their receptors (IGF-I receptor, IGF-IR; IGF-II/mannose 6-phosphate receptor, IGF-II/M6-PR), and six high affinity IGF binding proteins (IGFBPs) participate in the regulation of growth and differentiation of cells of the fibroblast lineage, possibly contributing to the fibrogenic process. The aim of this work was to study the expression and regulation of the IGF axis components in rat liver MF. Methods: Cultures of MF from passages I to 4 (P1-4) were studied. IGFBP secretion was analyzed by [I-125]-IGF-I ligand and immunoblotting. IGF-I, IGF-IR, IGF-II/M6-PR, and IGFBP messenger RNA (mRNA) expression was assessed by Northern blot hybridization. DNA synthesis was evaluated by 5-bromo-2'-deoxyuridine (BrdU) incorporation assay. Results: MF from PI to 4 constitutively expressed nnRNA transcripts specific for IGF-I, IGF-IR, and IGF-II/M6-PR. In MF, biosynthesis of IGFBP-3 and -2 was observed that was stimulated by IGF-I, insulin, and transforming growth factor P (TGF-beta), whereas platelet-derived growth factor (PDGF-BB) revealed inhibitory effects. IGF-I and to a lesser extent insulin increased DNA synthesis of MF. Simultaneous addition of recombinant human IGFBP-2 or -3 with IGF-I diminished the mitogenic effect of IGF-I on MF whereas preincubation of MF with IGFBP-2 or -3 further potentiated the IGF-I stimulated DNA synthesis. In conclusion, the present study demonstrates that the IGF axis may play a role in the regulation of MF proliferation in vitro which might be relevant in vivo for the process of fibrogenesis during acute and chronic liver injury. J. Cell. Physiol. 199: 388-398, 2004. (C) 2004 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/jcp.10437"],["dc.identifier.isi","000221180200007"],["dc.identifier.pmid","15095286"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48218"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0021-9541"],["dc.title","Expression and regulation of the insulin-like growth factor axis components in rat liver myofibroblasts"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","72"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Hepatology"],["dc.bibliographiccitation.lastpage","80"],["dc.bibliographiccitation.volume","45"],["dc.contributor.author","Tron, Kyrylo"],["dc.contributor.author","Samoylenko, Aantoly"],["dc.contributor.author","Musikowski, Gernot"],["dc.contributor.author","Kobe, Fritz"],["dc.contributor.author","Immenschuh, Stephan"],["dc.contributor.author","Schaper, Fred"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Kietzmann, Thomas"],["dc.date.accessioned","2018-11-07T09:36:49Z"],["dc.date.available","2018-11-07T09:36:49Z"],["dc.date.issued","2006"],["dc.description.abstract","Background/Aims: Heme oxygenase-1 (HO-1) can be induced by various stimuli, one of which is interleukin-6 (IL-6). Therefore, the aim of this study was to elucidate the molecular mechanisms responsible for IL-6-dependent HO-1 induction in the liver. Methods: The IL-6-dependent HO-1 regulation in rat primary hepatocytes and HepG2 hepatoma cells was studied by Northern and Western blot analyses, HO-1 promoter reporter gene assays and EMSA. Results: The HO-1 expression was transcriptionally induced by IL-6 in a time- and dose-dependent manner. Activation of signal transducers and activators of transcription (STAT) factors by the IL-6 receptor was crucial for HO-1 induction. By contrast, negative regulation of HO-1 expression appeared to be mediated through the SH2-domain-containing tyrosine phosphatase-2 (SHP2)/suppressors of cytokine signaling-3 (SOCS3) binding site within the gp130 IL-6 receptor subunit. Among the three putative STAT binding elements (SBE) in the HO-1 promoter, only the distal one was functional and when deleted, the remaining Luc induction was completely obliterated by the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002. Conclusions: The HO-1 SBE3 mediates HO-1 gene induction by IL-6 mainly via activation of the Jak/STAT pathway. (c) 2006 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jhep.2005.12.019"],["dc.identifier.isi","000238782200010"],["dc.identifier.pmid","16510205"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32701"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0168-8278"],["dc.title","Regulation of rat heme oxygenase-1 expression by interleukin-6 via the Jak/STAT pathway in hepatocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","51"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Growth Hormone & IGF Research"],["dc.bibliographiccitation.lastpage","60"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Novosyadlyy, R."],["dc.contributor.author","Lelbach, A."],["dc.contributor.author","Sheikh, Nadeem"],["dc.contributor.author","Tron, Kyrylo"],["dc.contributor.author","Pannem, Rajeswararao"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Scharf, Jens-Gerd"],["dc.date.accessioned","2018-11-07T08:33:03Z"],["dc.date.available","2018-11-07T08:33:03Z"],["dc.date.issued","2009"],["dc.description.abstract","Objective: The acute-phase response (APR), a cytokine-induced defense reaction of the body that enhances the innate immunity mechanisms directed to eliminate the noxious agent and restrict the area of damage, is accompanied by numerous alterations of the IGF axis. The liver is it central organ of both the IGF system and the APR because it releases most of IGF-I and IGFBP-1 in the circulation and is the main target organ for acute-phase-cytokines such its IL-6. Methods: In the Current work the expression of IGF-I and IGFBP-1 was studied in the liver and extrahepatic tissues in it rat model of localized inflammation induced by intramuscular injection Of turpentine oil (TO). The mRNA expression of IGF-I and IGFBP-1 was determined by Northern blot analysis and quantitative RT-PCR. Circulating levels of IGF-I and IGFBP-1 were evaluated by radioimmunoassay and [(125)I]-IGF-I ligand blotting, respectively. Results: Administration of TO to the rats led to it significant reduction of IGF-I gene expression in the liver and spleen. These changes were accompanied by a reduction of serum IGF-I concentrations to approximately 50% of levels observed in control rats. In contrast to IGF-I, IGFBP-1 mRNA expression was rapidly elevated in the livers of TO-treated rats. IGFBP-1 transcripts were already detectable at 30 min after TO injection and reached their maximal levels by 6 h. IGFBP-1 gene expression was also increased in the kidneys. This elevation, however, was delayed and less prominent than in the liver. Conclusions: Our data demonstrate that localized inflammation induced by intramuscular TO injection is accompanied not only by decreased IGF-I but also by increased IGFBP-1 gene expression explaining at least in part the catabolic changes of metabolism observed during the acute-phase response. (C) 2008 Elsevier Ltd. All rights reserved."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [GRK 335/2]"],["dc.identifier.doi","10.1016/j.ghir.2008.05.004"],["dc.identifier.isi","000263712300006"],["dc.identifier.pmid","18632293"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17483"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Churchill Livingstone"],["dc.relation.issn","1096-6374"],["dc.title","Temporal and spatial expression of IGF-I and IGFBP-1 during acute-phase response induced by localized inflammation in rats"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","800"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Laboratory Investigation"],["dc.bibliographiccitation.lastpage","814"],["dc.bibliographiccitation.volume","86"],["dc.contributor.author","Sheikh, Nadeem"],["dc.contributor.author","Tron, Kyrylo"],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T09:29:52Z"],["dc.date.available","2018-11-07T09:29:52Z"],["dc.date.issued","2006"],["dc.description.abstract","The source of serum cytokine-induced neutrophil chemoattractant ( CINC-1) and consequences of its presence in the tissue of synthesis have not been clearly elucidated under acute-phase situation. To pursue this question, turpentine oil ( TO) was intramuscularly injected into rats, and RNA and local protein levels of acute-phase cytokines and of CINC-1 were studied in the TO injected gluteal muscle, as well as in noninjured muscle, in the liver, kidney, lung and spleen. The serum levels of acute-phase mediators and of CINC-1 were measured together with total leukocyte subpopulations. Recruitment of inflammatory cells in muscle and in the other organs was investigated by quantitative immunohistochemical methods. The effect of acute-phase mediators, including interferon gamma ( IFN-gamma) on the synthesis of CINC-1 in cultured hepatocytes was also investigated at the RNA and protein level. We found that the sera of the TO-treated rats contained elevated levels of IL-6, IL-1 beta and CINC-1. Increased serum levels of IFN-gamma were also observed not only in the injured muscle but also and to a higher extent in the liver. However, while neutrophils and mononuclear phagocytes were found in the injured muscle, no inflammatory cells were detected at the non-'inflamed' site, namely, the liver or in the other organs. In vitro, treatment of cultured hepatocytes with IL-1 beta led to elevated CINC-1 gene expression. This was true to a lesser extent upon IL-6 and tumor necrosis factor ( TNF-alpha) exposure. Interestingly, IFN-gamma did not effect CINC-1 gene expression. These results indicate that CINC-1 behaves as an acute-phase protein and its expression is inducible in hepatocytes. However, CINC-1-production in the liver does not lead to recruitment of inflammatory cells into the organ."],["dc.identifier.doi","10.1038/labinvest.3700435"],["dc.identifier.isi","000239201300006"],["dc.identifier.pmid","16715102"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31158"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0023-6837"],["dc.title","Cytokine-induced neutrophil chemoattractant-1 is released by the noninjured liver in a rat acute-phase model"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","G482"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","AJP Gastrointestinal and Liver Physiology"],["dc.bibliographiccitation.lastpage","G490"],["dc.bibliographiccitation.volume","291"],["dc.contributor.author","Sheikh, Nadeem"],["dc.contributor.author","Batusic, Danko S."],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","Tron, Kyrylo"],["dc.contributor.author","Neubauer, Katrin"],["dc.contributor.author","Saile, Bernhard"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T09:16:47Z"],["dc.date.available","2018-11-07T09:16:47Z"],["dc.date.issued","2006"],["dc.description.abstract","In this work, we used two rat models, partial hepatectomy (PH) and CCl4 administration, to study the changes in iron pathways in response to hepatic damage. Liver injury induced changes in the hepatic gene expression of hepcidin, hemojuvelin (Hjv), several other proteins of iron metabolism, and several cytokines such as IL-1 beta IL-6, TNF-alpha, and IFN-gamma. Hepcidin gene expression was upregulated between 4 and 8 h with a maximum up to 16 h after surgery. However, Hjv gene expression was downregulated at the same time. An early upregulation of hepcidin ( 3 h) and downregulation of Hjv gene expression was found after CCl4 administration. Transferrin receptor 1 and ferritin H gene expression was upregulated, whereas ferroportin 1 gene expression was downregulated. Hepatic IL-6 gene expression was upregulated early after PH and reached maximum 8 h after the PH. In CCl4-induced liver injury, IL-6, IL-1 beta, TNF-alpha, and IFN-gamma upregulation were found at the maximum 12 h after the administration of the toxin. Treatment of isolated rat hepatocytes with IL-6 and, to a lesser extent, with IL-1 beta but not with TNF-alpha or IFN-gamma dose dependently upregulated hepcidin and downregulated Hjv gene expression. In hepatic damage, changes of the hepatic gene expression of the main proteins involved in iron metabolism may be induced by locally synthesized mediators."],["dc.identifier.doi","10.1152/ajpgi.00586.2005"],["dc.identifier.isi","000239679600014"],["dc.identifier.pmid","16574981"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28013"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Physiological Soc"],["dc.relation.issn","0193-1857"],["dc.title","Hepcidin and hemojuvelin gene expression in rat liver damage: in vivo and in vitro studies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S134"],["dc.bibliographiccitation.journal","Journal of Hepatology"],["dc.bibliographiccitation.lastpage","S135"],["dc.bibliographiccitation.volume","44"],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","Elmaouhoub, Abderrahim"],["dc.contributor.author","Mansuroglu, Tuemen"],["dc.contributor.author","Batusic, D."],["dc.contributor.author","Papoutsi, Maria"],["dc.contributor.author","Tron, Kyrylo"],["dc.contributor.author","Saile, Bernhard"],["dc.contributor.author","Wilting, J."],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T10:36:24Z"],["dc.date.available","2018-11-07T10:36:24Z"],["dc.date.issued","2006"],["dc.identifier.doi","10.1016/S0168-8278(06)80352-1"],["dc.identifier.isi","000237328100352"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45313"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","41st Annual Meeting of the European-Association-for-the-Study-of-the-Liver"],["dc.relation.eventlocation","Vienna, AUSTRIA"],["dc.relation.issn","0168-8278"],["dc.title","Analysis of the homeobox transcription factor Prox-1 expression in rat liver development and in different models of liver damage and regeneration"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","638"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Hepatology"],["dc.bibliographiccitation.lastpage","645"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Armbrust, T."],["dc.contributor.author","Kreissig, M."],["dc.contributor.author","Tron, Kyrylo"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T10:49:59Z"],["dc.date.available","2018-11-07T10:49:59Z"],["dc.date.issued","2004"],["dc.description.abstract","Background/Aims: In acute liver injury, fibronectin (FN) is deposited at the site of hepatocellular necrosis. We have previously shown that liver inflammatory mononuclear phagocytes (MNP), in contrast to quiescent hepatic macrophages, synthesize abundant amounts of FN. We now analyzed effects of agents known to influence macrophage functions to better understand liver damage and repair. Methods: Acute rat liver injury was induced by CCl4. Liver cellular FN (cFN) expression was analyzed by in situ-hybridization. Liver MNP were isolated and characterized immunocytochemically. Protein synthesis was studied by biosynthetic labeling, immunoprecipitation, and SDS-PAGE. RNA was analyzed by Northern Blotting. Results: cFN gene expression was localized by in situ-hybridization and immunohistochemistry within the pericentral inflammatory infiltrate. Treatment of inflammatory MNP with dexamethasone, or interferon-gamma, or lipopolysaccharide induced a dose-dependent decrease in cFN gene expression, whereas transforming growth factor-P increased cFN gene expression. Conclusions: 1. Inflammatory MNP express cFN. 2. Downregulation of cFN expression by dexamethasone in inflammatory MNP may explain delayed wound healing after corticosteroid therapy. Interferon-gamma and lipopolysaccharide could also delay the repair process in the liver. Transforming growth factor-beta may promote liver wound healing after acute liver injury by increasing local cFN synthesis in inflammatory mononuclear phagocytes of the inflammatory infiltrate. (C) 2004 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jhep.2003.12.013"],["dc.identifier.isi","000220641200010"],["dc.identifier.pmid","15030980"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48554"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0168-8278"],["dc.title","Modulation of fibronectin gene expression in inflammatory mononuclear phagocytes of rat liver after acute liver injury"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","549"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Histochemistry and Cell Biology"],["dc.bibliographiccitation.lastpage","562"],["dc.bibliographiccitation.volume","126"],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","Elmaouhoub, Abderrahim"],["dc.contributor.author","Mansuroglu, Tuemen"],["dc.contributor.author","Batusic, Danko"],["dc.contributor.author","Tron, Kyrylo"],["dc.contributor.author","Saile, Bernhard"],["dc.contributor.author","Papoutsi, Maria"],["dc.contributor.author","Pieler, Tomas"],["dc.contributor.author","Wilting, Joerg"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T09:01:16Z"],["dc.date.available","2018-11-07T09:01:16Z"],["dc.date.issued","2006"],["dc.description.abstract","The aim of this study was to analyse the changes of Prospero-related homeobox 1 (Prox1) gene expression in rat liver under different experimental conditions of liver injury, regeneration and acute phase reaction, and to correlate it with that of markers for hepatoblasts, hepatocytes, cholangiocytes and oval cells. Gene expression was studied at RNA level by RT-PCR, and at protein level by immunohistochemistry. At embryonal stage of rat liver development (embryonal days (ED) 14-16) hepatoblasts were found to be Prox1(+)/Cytokeratin (CK) 19(+) and alpha-fetoprotein (AFP)(+), at this stage Prox1(-)/CK19(+)/AFP(-) small cells (early cholangiocytes?) were identified. In fetal liver (ED 18-22) hepatoblasts were Prox1(+)/CK19(-)/AFP(+). CK7(+) cholangiocytes were detected at this stage, and they were Prox1(-)/AFP(-). In the adult liver hepatocytes were Prox1(+)/CK19(-)/CK7(-)/AFP(-), cholangiocytes were CK19(+) and/or CK7(+) and AFP(-)/Prox1(-). In models of liver damage and regeneration Prox1 remained a stable marker of hepatocytes. After 2-acetyl-aminofluorene treatment with partial hepatectomy (AAF/PH) the amount of Prox1 specific transcripts was low in the liver, when CK19 and AFP gene expression was high, and at no time point AFP(+)/CK19(+) \"oval cells\" were found to be Prox1(+). However, a few Prox1(+)/CK19(+) and a few Prox1(+)/CK7(+) cells were identified in the liver of AAF/PH-animals, which may represent precursors of hepatocytes, or a precancerous state."],["dc.identifier.doi","10.1007/s00418-006-0191-4"],["dc.identifier.isi","000240980900003"],["dc.identifier.pmid","16770575"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24380"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0948-6143"],["dc.title","Prospero-related homeobox 1 (Prox1) is a stable hepatocyte marker during liver development, injury and regeneration, and is absent from \"oval cells\""],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","245"],["dc.bibliographiccitation.issue","3-4"],["dc.bibliographiccitation.journal","Histochemistry and Cell Biology"],["dc.bibliographiccitation.lastpage","260"],["dc.bibliographiccitation.volume","124"],["dc.contributor.author","Batusic, Danko S."],["dc.contributor.author","Cimica, Velasco"],["dc.contributor.author","Chen, Y. L."],["dc.contributor.author","Tron, Kyrylo"],["dc.contributor.author","Hollemann, T."],["dc.contributor.author","Pieler, T."],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T10:56:11Z"],["dc.date.available","2018-11-07T10:56:11Z"],["dc.date.issued","2005"],["dc.description.abstract","Under certain conditions liver regeneration can be accomplished by hepatic progenitor cells (\"oval cells\"). So far, only few factors have been identified to be uniquely regulated by the \"oval cell\" compartment. Using macroarray analysis in a rat model of oval cell proliferation (treatment with 2-acetylaminofluorene and partial hepatectomy, AAF + PH), we identified 12 differentially expressed genes compared to appropriate control models (AAF treatment and sham operation or AAF treatment alone). Further analysis in models of normal liver regeneration (ordinary PH) and acute phase response (turpentine oil-treated rats) revealed that three out of 12 genes (thymidine kinase 1, Jun-D and ADP-ribosylation factor 4) were not affected by the hepatic acute phase reaction but similarly overexpressed in both \"oval cell\" -dependant and normal liver regeneration. We characterized Jun-D and ADP-ribosylation factors as novel factors upregulated in oval cells and in nonparenchymal liver cells of normally regenerating livers. However, two out of 12 differentially expressed genes were specifically expressed in oval cells: ras-related protein Rab-3b and Ear-2. On protein level, Rab-3b was increased in total liver homogenates and demonstrated only in clusters of oval cells. We postulate that Ear-2 and Rab-3b may represent novel regulatory factors specifically activated in \"oval cells\"."],["dc.identifier.doi","10.1007/s00418-005-0021-0"],["dc.identifier.isi","000233012600007"],["dc.identifier.pmid","16044259"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49955"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0948-6143"],["dc.title","Identification of genes specific to rat 2-acetylaminofluorene/partial 'oval cells\" in the hepatectomy model"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","376"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Laboratory Investigation"],["dc.bibliographiccitation.lastpage","387"],["dc.bibliographiccitation.volume","85"],["dc.contributor.author","Tron, Kyrylo"],["dc.contributor.author","Novosyadlyy, R."],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","Samoylenko, A."],["dc.contributor.author","Kietzmann, Thomas"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T11:20:55Z"],["dc.date.available","2018-11-07T11:20:55Z"],["dc.date.issued","2005"],["dc.description.abstract","Heme oxygenase- 1 ( HO- 1) is the inducible isoform of an enzyme family responsible for heme degradation and was suggested to be involved in the acute phase response in the liver. However, the mechanisms of the HO- 1 regulation under inflammatory conditions are poorly understood. Therefore, the purpose of the current work was to study the expression of HO- 1 in the liver and other organs of rats with a localized inflammation after intramuscular injection of turpentine oil ( TO). Since interleukin- 6 ( IL- 6) is known to be a principal mediator of inflammation, the levels of this cytokine were also estimated in the animal model used. HO- 1 and IL- 6 expression was evaluated by Northern blot, in situ hybridization, Western blot, immunohistochemistry and enzyme- linked immunosorbent assay. In the liver and injured muscle, the HO- 1 mRNA levels were dramatically increased 4 - 6 h after TO administration. HO- 1 protein levels in the liver were elevated starting from 6 - 12 h after the treatment. In other internal organs such as the heart, kidney and large intestine, only a slight induction of HO- 1 mRNA was observed. IL- 6- specific transcripts appeared only in the injured muscle and were in accordance with serum levels of IL- 6. In turn, temporal expression of IL- 6 in the muscle and circulatory IL- 6 levels correlated well with HO- 1 expression in the liver and injured muscle. In the liver of control rats HO- 1 protein was detected in Kupffer cells, while in TO- injected rats also hepatocytes became strongly HO- 1 positive. Conversely, in the injured muscle, HO- 1 immunoreactivity was attributed only to macrophages. Our data demonstrate that during localized inflammation HO- 1 expression was rapidly and strongly induced in macrophages of injured muscle and in hepatocytes, and IL- 6 derived from injured muscle seems to be responsible for the HO- 1 induction in the liver."],["dc.identifier.doi","10.1038/labinvest.3700228"],["dc.identifier.isi","000227168700008"],["dc.identifier.pmid","15640832"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55649"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1530-0307"],["dc.relation.issn","0023-6837"],["dc.title","Upregulation of heme oxygenase-1 gene by turpentine oil-induced localized inflammation: involvement of interleukin-6"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]