Ramadori, Giuliano

[["dc.bibliographiccitation.firstpage","389"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Radiation and Environmental Biophysics"],["dc.bibliographiccitation.lastpage","397"],["dc.bibliographiccitation.volume","47"],["dc.contributor.author","Tello, Khodr"],["dc.contributor.author","Christiansen, H."],["dc.contributor.author","Guerleyen, Hakan"],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Hess, C. F."],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Saile, Bernhard"],["dc.date.accessioned","2018-11-07T11:13:47Z"],["dc.date.available","2018-11-07T11:13:47Z"],["dc.date.issued","2008"],["dc.description.abstract","In a previous publication, we were able to show that irradiation of Kupffer cells, the liver resident macrophages, leads to an increased TNF-alpha concentration in the culture medium. The pathomechanisms underlying this phenomenon, however, remained to be elucidated. Here, we show that following irradiation of Kupffer cells, the apoptosis rate increased drastically within 48 h. At the same time, the total TNF-alpha concentration in cell lysates of Kupffer cells attached to the culture plate decreased. However, normalization of the TNF-alpha concentration with respect to cell number revealed that TNF-alpha concentration per attached cell remained constant during the observation period. Western blot analysis showed that heat shock protein 27 (Hsp27) is strongly downregulated and bax is upregulated in irradiated Kupffer cells as compared to sham-irradiated cells. Overexpression of Hsp27 in Kupffer cells was shown to prevent the effect of irradiation on bax expression, apoptosis and, at the same time, on increase of TNF-alpha concentration in the Kupffer cell medium. We conclude that irradiation of Kupffer cells leads to apoptosis because of downregulation of Hsp27 and consecutive upregulation of bax expression. Furthermore, we suggest that apoptosis of Kupffer cells leads to an increase of TNF-alpha concentration in the culture medium which may be due to cell death rather than active release or synthesis."],["dc.identifier.doi","10.1007/s00411-008-0170-3"],["dc.identifier.isi","000256763500012"],["dc.identifier.pmid","18493784"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/3099"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53980"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1432-2099"],["dc.relation.issn","0301-634X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Irradiation leads to apoptosis of Kupffer cells by a Hsp27-dependant pathway followed by release of TNF-alpha"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","BMC physiology"],["dc.bibliographiccitation.lastpage","14"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Neubauer, Katrin"],["dc.contributor.author","Lindhorst, Alexander"],["dc.contributor.author","Tron, Kyrylo"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Saile, Bernhard"],["dc.date.accessioned","2019-07-10T08:12:56Z"],["dc.date.available","2019-07-10T08:12:56Z"],["dc.date.issued","2008"],["dc.description.abstract","Background and aim: The mechanisms of transmigration of inflammatory cells through the sinusoids are still poorly understood. This study aims to identify in vitro conditions (cytokine treatment) which may allow a better understanding of the changes in PECAM (platelet endothelial cell adhesion molecule)-1-gene-expression observed in vivo. Methods and results: In this study we show by immunohistochemistry, that there is an accumulation of ICAM-1 (intercellular cell adhesion molecule-1) and ED1 positive cells in necrotic areas of livers of CCl4-treated rats, whereas there are few PECAM-1 positive cells observable. After the administration of CCl4, we could detect an early rise of levels of IFN-? followed by an enhanced TGF-? protein level. As shown by Northern blot analysis and surface protein expression analysed by flow cytometry, IFN-?-treatment decreased PECAM-1-gene-expression in isolated SECs (sinusoidal endothelial cells) and mononuclear phagocytes (MNPs) in parallel with an increase in ICAM-1-gene-expression in a dose and time dependent manner. In contrast, TGF-?-treatment increased PECAM-1-expression. Additional administration of IFN-? to CCl4-treated rats and observations in IFN-?-/- mice confirmed the effect of IFN-? on PECAM-1 and ICAM-1-expression observed in vitro and increased the number of ED1-expressing cells 12 h after administration of the toxin.Conclusion: The early decrease of PECAM-1-expression and the parallel increase of ICAM-1-expression following CCl4-treatment is induced by elevated levels of IFN-? in livers and may facilitate adhesion and transmigration of inflammatory cells. The up-regulation of PECAM-1-expression in SECs and MNPs after TGF-?-treatment suggests the involvement of PECAM-1 during the recovery after liver damage."],["dc.identifier.fs","204399"],["dc.identifier.ppn","575631112"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/4335"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61081"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1472-6793"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","616"],["dc.title","Decrease of PECAM-1-gene-expression induced by proinflammatory cytokines IFN-Ú and IFN-» is reversed by TGF-Ø in sinusoidal endothelial cells and hepatic mononuclear phagocytes"],["dc.title.alternative","Research article"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","449"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Cell and Tissue Research"],["dc.bibliographiccitation.lastpage","462"],["dc.bibliographiccitation.volume","337"],["dc.contributor.author","Piscaglia, Fabio"],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","Knittel, Thomas"],["dc.contributor.author","Di Rocco, Paola"],["dc.contributor.author","Kobold, Dominik"],["dc.contributor.author","Saile, Bernhard"],["dc.contributor.author","Zocco, Maria Assunta"],["dc.contributor.author","Timpl, Rupert"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T11:24:35Z"],["dc.date.available","2018-11-07T11:24:35Z"],["dc.date.issued","2009"],["dc.description.abstract","Fibulin-2 has previously been considered as a marker to distinguish rat liver myofibroblasts from hepatic stellate cells. The function of other fibulins in acute or chronic liver damage has not yet been investigated. The aim of this study has been to evaluate the expression of fibulin-1 and -2 in models of rat liver injury and in human liver cirrhosis. Their cellular sources have also been investigated. In normal rat liver, fibulin-1 and -2 were both mainly present in the portal field. Fibulin-1-coding transcripts were detected in total RNA of normal rat liver, whereas fibulin-2 mRNA was only detected by sensitive, real-time quantitative polymerase chain reaction. In acute liver injury, the expression of fibulin-1 was significantly increased (17.23-fold after 48 h), whereas that of fibulin-2 was not modified. The expression of both fibulin-1 and -2 was increased in experimental rat liver cirrhosis (19.16- and 26.47-fold, respectively). At the cellular level, fibulin-1 was detectable in hepatocytes, \"activated\" hepatic stellate cells, and liver myofibroblasts (2.71-, 122.65-, and 469.48-fold over the expression in normal rat liver), whereas fibulin-2 was restricted to liver myofibroblasts and was regulated by transforming growth factor beta-1 (TGF-beta 1) in 2-day-old hepatocyte cultures and in liver myofibroblasts. Thus, fibulin-1 and -2 respond differentially to single and repeated damaging noxae, and their expression is differently present in liver cells. Expression of the fibulin-2 gene is regulated by TGF-beta 1 in liver myofibroblasts."],["dc.description.sponsorship","SFB [402]"],["dc.identifier.doi","10.1007/s00441-009-0823-9"],["dc.identifier.isi","000269055200009"],["dc.identifier.pmid","19609566"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/3540"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56440"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0302-766X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Expression of ECM proteins fibulin-1 and-2 in acute and chronic liver disease and in cultured rat liver cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","85"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Radiation and Environmental Biophysics"],["dc.bibliographiccitation.lastpage","94"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Guerleyen, Hakan"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Tello, Khodr"],["dc.contributor.author","Dudas, Joszef"],["dc.contributor.author","Hermann, Robert Michael"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Saile, Bernhard"],["dc.date.accessioned","2018-11-07T08:33:19Z"],["dc.date.available","2018-11-07T08:33:19Z"],["dc.date.issued","2009"],["dc.description.abstract","This study aimed to reveal the pathophysiological signalling responsible for radiation-induced sensitization of hepatocytes to TNF-alpha-mediated apoptosis. I kappa B was upregulated in irradiated hepatocytes. Administration of I kappa B antisense oligonucleotides prior to irradiation inhibited occurrence of apoptosis after TNF-alpha administration. Caspases-8, -9 and -3 activities were increased in irradiated hepatocytes and downregulation of apoptosis by I kappa B antisense oligonucleotides was mediated by suppression of caspases-9 and -3 activation but not of caspase-8 activation, suggesting that radiation-induced sensitization of hepatocytes to TNF-alpha-mediated apoptosis additionally requires changes upstream of caspase-8 activation. Herein, upregulation of FLIP may play a crucial role. Cleavage of bid, upregulation of bax, downregulation of bcl-2 and release of cytochrome c after TNF-alpha-administration depend on radiation-induced upregulation of I kappa B, thus demonstrating an apoptosis permitting effect of I kappa B."],["dc.description.sponsorship","Deutsche Krebshilfe [106760]"],["dc.identifier.doi","10.1007/s00411-008-0200-1"],["dc.identifier.isi","000262316300009"],["dc.identifier.pmid","18956207"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/3523"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17548"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1432-2099"],["dc.relation.issn","0301-634X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Irradiation leads to sensitization of hepatocytes to TNF-alpha-mediated apoptosis by upregulation of I kappa B expression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]