Lindhorst, Alexander

[["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","265"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Histochemistry and Cell Biology"],["dc.bibliographiccitation.lastpage","275"],["dc.bibliographiccitation.volume","120"],["dc.contributor.author","Neubauer, K."],["dc.contributor.author","Baruch, Y."],["dc.contributor.author","Lindhorst, Alexander"],["dc.contributor.author","Saile, Bernhard"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T10:35:47Z"],["dc.date.available","2018-11-07T10:35:47Z"],["dc.date.issued","2003"],["dc.description.abstract","Gelsolin, a 90-kDa protein, was suggested to be involved in cell motility, to inhibit apoptosis and to have a protective role for tissue. This study intends to analyse the modulation of cytoplasmic gelsolin expression in damaged rat and human livers and to identify its cellular sources. In the normal liver gelsolin-immunoreactive cells could be identified along vessel walls and along the sinusoids. In cultured rat hepatic stellate cells (HSCs), liver myofibroblasts (MFs), mononuclear cells (MCs) and sinusoidal endothelial cells (SECs), but not in hepatocytes, gelsolin expression could be detected by immunostaining and Northern blot analysis. In acute CCl4-induced liver damage there was no gelsolin positivity detectable in necrotic areas. However, in human fulminant hepatic failure positivity in the necrotic areas was detected. In chronically damaged rat and human livers gelsolin-immunoreactive cells could be identified within the fibrotic septa. Northern blot analysis revealed an increase of the gelsolin-specific transcript level under conditions of acute and chronic human or rat liver damage. The amount of gelsolin-specific transcripts in SECs and large MCs isolated from damaged rat livers increased in comparison to cells obtained from normal rats. However, the amount of gelsolin-specific transcripts in small MCs (representing recruited inflammatory cells) decreased. In conclusion, SECs, MCs, MFs and HSCs, but not hepatocytes, express gelsolin. In the damaged liver all tested cell populations but the inflammatory cells and the hepatocytes are responsible for the enhanced gelsolin expression."],["dc.identifier.doi","10.1007/s00418-003-0564-x"],["dc.identifier.isi","000186082500002"],["dc.identifier.pmid","14574581"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45172"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0948-6143"],["dc.title","Gelsolin gene expression is upregulated in damaged rat and human livers within non-parenchymal cells and not in hepatocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]