Krause, Petra

[["dc.bibliographiccitation.firstpage","723"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Histochemistry and Cell Biology"],["dc.bibliographiccitation.lastpage","734"],["dc.bibliographiccitation.volume","126"],["dc.contributor.author","Koenig, Sarah"],["dc.contributor.author","Probst, Irmelin"],["dc.contributor.author","Becker, Heinz"],["dc.contributor.author","Krause, Petra"],["dc.date.accessioned","2018-11-07T08:53:50Z"],["dc.date.available","2018-11-07T08:53:50Z"],["dc.date.issued","2006"],["dc.description.abstract","Oval cells constitute a heterogeneous population of proliferating progenitors found in rat livers following carcinogenic treatment (2-acetylaminofluorene and 70% hepatectomy). The aim of this study was to investigate the cellular pattern of various differentiation and cell type markers in this model of liver regeneration. Immunophenotypic characterisation revealed at least two subtypes emerging from the portal field. First, a population of oval cells formed duct-like structures and expressed bile duct (CD49f) as well as hepatocytic markers (alpha-foetoprotein, CD26). Second, a population of non-ductular oval cells was detected between and distally from the ductules expressing the neural marker nestin and the haematopoietic marker Thy1. Following oval cell isolation, a subset of the nestin-positive cells was shown to co-express hepatocytic and epithelial markers (albumin, CD26, pancytokeratin) and could be clearly distinguished from anti-desmin reactive hepatic stellate cells. The gene expression profiles (RT-PCR) of isolated oval cells and oval cell liver tissue were found to be similar to foetal liver (ED14). The present results suggest that the two oval cell populations are organised in a zonal hierarchy with a marker gradient from the inner (displaying hepatocytic and biliary markers) to the outer zone (showing hepatocytic and extrahepatic progenitor markers) of the proliferating progeny clusters."],["dc.identifier.doi","10.1007/s00418-006-0204-3"],["dc.identifier.isi","242624400009"],["dc.identifier.pmid","16835754"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22524"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0948-6143"],["dc.title","Zonal hierarchy of differentiation markers and nestin expression during oval cell mediated rat liver regeneration"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","581"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Histochemistry and Cell Biology"],["dc.bibliographiccitation.lastpage","591"],["dc.bibliographiccitation.volume","135"],["dc.contributor.author","Doratiotto, Silvia"],["dc.contributor.author","Krause, Petra"],["dc.contributor.author","Serra, Maria Paola"],["dc.contributor.author","Marongiu, Fabio"],["dc.contributor.author","Sini, Marcella"],["dc.contributor.author","Koenig, Sarah"],["dc.contributor.author","Laconi, Ezio"],["dc.date.accessioned","2018-11-07T08:55:35Z"],["dc.date.available","2018-11-07T08:55:35Z"],["dc.date.issued","2011"],["dc.description.abstract","Overt neoplasia is often the end result of a long biological process beginning with the appearance of focal lesions of altered tissue morphology. While the putative clonal nature of focal lesions has often been emphasized, increasing attention is being devoted to the possible role of an altered growth pattern in the evolution of carcinogenesis. Here we compare the growth patterns of normal and nodular hepatocytes in a transplantation system that allows their selective clonal proliferation in vivo. Rats were pre-treated with retrorsine, which blocks the growth of resident hepatocytes, and were then transplanted with hepatocytes isolated from either normal liver or hepatocyte nodules. Both cell types were able to proliferate extensively in the recipient liver, as expected. However, their growth pattern was remarkably different. Clusters of normal hepatocytes integrated in the host liver, displaying a normal histology; however, transplanted nodular hepatocytes formed new hepatocyte nodules, with altered morphology and sharp demarcation from surrounding host liver. Both the expression and distribution of proteins involved in cell polarity, cell communication, and cell adhesion, including connexin 32, E-cadherin, and matrix metalloproteinase-2, were altered in clusters of nodular hepatocytes. Furthermore, we were able to show that down-regulation of connexin 32 and E-cadherin in nodular hepatocyte clusters was independent of growth rate. These results support the concept that a dominant pathway towards neoplastic disease in several organs involves defect(s) in tissue pattern formation."],["dc.description.sponsorship","AIRC (Italian Association for Cancer Research) [4927, 10604]"],["dc.identifier.doi","10.1007/s00418-011-0813-3"],["dc.identifier.isi","000291222300005"],["dc.identifier.pmid","21528371"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6622"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22939"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0948-6143"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","The growth pattern of transplanted normal and nodular hepatocytes"],["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","1214"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Journal of Pediatric Surgery"],["dc.bibliographiccitation.lastpage","1219"],["dc.bibliographiccitation.volume","39"],["dc.contributor.author","Wilhelm, A."],["dc.contributor.author","Leister, Ingo"],["dc.contributor.author","Sabandal, P."],["dc.contributor.author","Krause, Petra"],["dc.contributor.author","Becker, H."],["dc.contributor.author","Markus, Peter M."],["dc.date.accessioned","2018-11-07T10:46:53Z"],["dc.date.available","2018-11-07T10:46:53Z"],["dc.date.issued","2004"],["dc.description.abstract","Background/Purpose: Over the last 20 years, hepatocyte transplantation (HcTx) has advanced from the experimental to the clinical stage. To date, HcTx has been performed in 30 patients in the United States. Regardless whether hepatocytes are transplanted into the spleen and migrate to the liver or are injected directly into the portal vein, transplanted liver cells will, to some extent, congest the recipient liver microcirculation. The potential negative consequences of intrasplenic HcTx were the subject of this study. Methods: By using intravital microscopy, the authors investigated whether intrasplenic HcTx of 20 X 10(6) allogenic hepatocytes would influence liver perfusion, excretory liver function, and nonparenchymal cells (Kupffer and Ito cells) in vivo. Results: The sinusoidal perfusion rate declined significantly from 94% (control) to 84% on day 1 and 76% on day 7. Bile acid excretion decreased in a similar fashion from 0.924 mg/h (control) to 0.669 mg/h on day 7. The authors observed a significant increase of Ito cells from 81.1 cells per microscopic field (control) to 97.1 (day 1) and an increase of Kupffer cells (KC; 6.1 cells per microscopic field on day 1 v3.8 on control). Conclusions: This study shows an acute impairment of hepatic microcirculation and hepatucellular function along with an recruitment and activation of nonparenchymal cells in the early posttransplantation period after intrasplenic HcTx. Kupffer cell recruitment indicates an activation of local host defense, and Ito cell activation implies the initiation of liver repair mechanisms owing to ischemia-related cell damage. (C) 2004 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.jpedsurg.2004.04.020"],["dc.identifier.isi","000223768400011"],["dc.identifier.pmid","15300530"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47845"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","W B Saunders Co"],["dc.relation.issn","0022-3468"],["dc.title","Acute impairment of hepatic microcirculation and recruitment of nonparenchymal cells by intrasplenic hepatocyte transplantation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","29"],["dc.bibliographiccitation.lastpage","39"],["dc.bibliographiccitation.seriesnr","1213"],["dc.contributor.author","Krause, Petra"],["dc.contributor.author","Rave-Frank, Margret"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Koenig, Sarah"],["dc.contributor.editor","Christ, Bruno"],["dc.contributor.editor","Oerlecke, Jana"],["dc.contributor.editor","Stock, Peggy"],["dc.date.accessioned","2021-06-02T10:44:23Z"],["dc.date.available","2021-06-02T10:44:23Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1007/978-1-4939-1453-1_3"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/87018"],["dc.notes.intern","DOI-Import GROB-425"],["dc.publisher","Springer New York"],["dc.publisher.place","New York, NY"],["dc.relation.crisseries","Methods in Molecular Biology"],["dc.relation.eisbn","978-1-4939-1453-1"],["dc.relation.isbn","978-1-4939-1452-4"],["dc.relation.ispartof","Methods in Molecular Biology"],["dc.relation.ispartof","Animal Models for Stem Cell Therapy"],["dc.relation.ispartofseries","Methods in Molecular Biology; 1213"],["dc.title","Preconditioning of the Liver for Efficient Repopulation by Primary Hepatocyte Transplants"],["dc.type","book_chapter"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","805"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Cell Transplantation"],["dc.bibliographiccitation.lastpage","817"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Krause, Petra"],["dc.contributor.author","Unthan-Fechner, Kirsten"],["dc.contributor.author","Probst, Irmelin"],["dc.contributor.author","Koenig, Sarah"],["dc.date.accessioned","2018-11-07T09:46:06Z"],["dc.date.available","2018-11-07T09:46:06Z"],["dc.date.issued","2014"],["dc.description.abstract","Clinical studies have proved the therapeutic potential of hepatocyte transplantation as a promising alternative to whole organ liver transplantation in the treatment of hereditary or end-stage liver disease. However, donor shortage seriously restricts cell availability, and the lack of appropriate cell culture protocols for the storage and maintenance of donor cells constitutes a significant obstacle. The aim of this study was to stimulate mature hepatocytes in culture to multiply in vitro and track their fate on transplantation. Rat hepatocytes isolated nonenzymatically were cultured serum free for up to 10 days. They were stimulated into proliferation in the presence of growth factors and conditioned media from nonparenchymal and hepatocyte culture supernatants, as well as 10 mM lithium chloride (LiCl). Cell proliferation was assessed by determining DNA content. Additionally, the extent of cell differentiation was estimated using immunofluorescence staining of hepatic, biliary, progenitor, and mesenchymal markers and gene expression analyses. Transplantation studies were performed on the Fischer CD26-mutant rat following pretreatment with retrorsine and partial hepatectomy. Proliferating hepatocytes increasingly adopted precursor characteristics, expressing progenitor (OV6, CD133), hepatic lineage (CK18), biliary (CD49f, CK7, CK19), and mesenchymal (vimentin) markers. The supplement of LiCl further enhanced the proliferative capacity by 30%. Transplantation studies revealed extensive repopulation by large donor hepatocyte clusters. Furthermore, bile duct-like structures deriving from donor cells proved to be immunoreactive to ductular markers and formed in close proximity to endogenous bile ducts. Mature hepatocytes reveal their potential to \"switch\" between phenotypes, adopting progenitor characteristics during proliferation in vitro. Following transplantation, these \"retrodifferentiated\" cells further expanded in vivo, thereby generating bipotentially differentiated progenies (hepatocytes and bile duct-like structures). This apparent plasticity of mature hepatocytes may open new approaches for cell-based strategies to treat liver disease."],["dc.identifier.doi","10.3727/096368913X664856"],["dc.identifier.isi","000337989700002"],["dc.identifier.pmid","23485196"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10644"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34784"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cognizant Communication Corp"],["dc.relation.issn","1555-3892"],["dc.relation.issn","0963-6897"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Cultured Hepatocytes Adopt Progenitor Characteristics and Display Bipotent Capacity to Repopulate the Liver"],["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","876"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","International Journal of Radiation Biology"],["dc.bibliographiccitation.lastpage","883"],["dc.bibliographiccitation.volume","90"],["dc.contributor.author","Serra, Maria Paola"],["dc.contributor.author","Marongiu, Fabio"],["dc.contributor.author","Sini, Marcella"],["dc.contributor.author","Marongiu, Michela"],["dc.contributor.author","Contini, Antonella"],["dc.contributor.author","Wolff, Hendrik"],["dc.contributor.author","Rave-Frank, Margret"],["dc.contributor.author","Krause, Petra"],["dc.contributor.author","Laconi, Ezio"],["dc.contributor.author","Koenig, Sarah"],["dc.date.accessioned","2018-11-07T09:34:32Z"],["dc.date.available","2018-11-07T09:34:32Z"],["dc.date.issued","2014"],["dc.description.abstract","Purpose: Exposure to radiation primes the liver for extensive replacement of the resident parenchymal cells by transplanted hepatocytes. The mechanisms underlying this repopulation remain to be clarified. In these studies, we examined the possible occurrence of cell senescence in vivo following radiationassociated preconditioning of the host liver. Materials and methods: Fischer 344 rats underwent externalbeam, computed-tomography-based partial liver irradiation. A single dose of 25 Gy was delivered to the right liver lobes (40% of liver mass). An additional group of animals received a 1/3 partial hepatectomy (removal of the left anterior lobe) four days after irradiation. Non-irradiated groups served as controls. All rats were sacrificed four weeks after the initial treatment. Results: The irradiated livers displayed several markers of cell senescence, including expression of senescence-associatedp-galactosidase (SA-I3-gal), increase in cell size, and up-regulation of cyclin-dependent kinase inhibitors (CDK-I) p16 and p21. Furthermore, quantitative reverse-transcriptase polyrnerase chain reaction (qRT-PCR) analysis revealed activation of the senescence-associated secretory phenotype (SAW), including the cytokines interleukin 6 (IL6) and le (ILla). The senescencerelated changes were more prominent in rats undergoing partial hepatectomy (PH) following irradiation (IR). Conclusions: We conclude that priming with radiation for liver repopulation results in the induction of cell senescence and the up-regulation of a senescence-associated secretory phenotype. The latter can contribute to the extensive growth of transplanted cells in this system."],["dc.identifier.doi","10.3109/09553002.2014.922714"],["dc.identifier.isi","000343001200006"],["dc.identifier.pmid","24827852"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32189"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Informa Healthcare"],["dc.relation.issn","1362-3095"],["dc.relation.issn","0955-3002"],["dc.title","Hepatocyte senescence induced by radiation and partial hepatectomy in rat liver"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","876"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Der Chirurg"],["dc.bibliographiccitation.lastpage","885"],["dc.bibliographiccitation.volume","76"],["dc.contributor.author","Langer, C."],["dc.contributor.author","Schwartz, P."],["dc.contributor.author","Krause, Petra"],["dc.contributor.author","Mohammadi, H."],["dc.contributor.author","Kulle, Bettina"],["dc.contributor.author","Schaper, A."],["dc.contributor.author","Fuzesi, Laszlo"],["dc.contributor.author","Becker, H."],["dc.date.accessioned","2018-11-07T10:55:59Z"],["dc.date.available","2018-11-07T10:55:59Z"],["dc.date.issued","2005"],["dc.description.abstract","Background. The biocompatibility of meshes in hernia surgery seems to be influenced markedly by the amount of the selected material and its structure. Fibroblasts play a major key role during the process of mesh incorporation. This study was performed to investigate differences in cell morphology and proliferation of human fibroblasts cultured on different polypropylene meshes. Methods. In the present in vitro study the cellular response of human fibroblasts was investigated by scanning electron microscopy (SEM), comparing three different polypropylene meshes: a newly constructed low-weight and microporous mesh (NK1), a low-weight and macroporous mesh with absorbable polyglactin filaments (Vypro), and a heavy-weight and microporous mesh (BiomeshP1). Human fibroblasts (1,5.105 cells) were incubated with the meshes (each 12 mm(2)) for 6 hours, 5 days, 2,4,6, and 12 weeks. Computer-assisted morphometry of the fibroblast/mesh surface ratio served to reflect the biological cell response. Results. The Vypro mesh showed the significantly highest fibroblast density during the first 6 weeks, but cell growth was nearly exclusively limited to the polyglactin filaments. At 3 months, after reabsorption of the polyglactin, the fibroblast-coated polypropylene mesh surface was only 50% compared to NK1 and BiomeshP1. The morphologic aspect of the fibroblasts on the BiomeshP1 mesh was much more degenerative and unphysiological, compared to NK1 and Vypro, with isolated, single cells instead of a broad, connective growth. The BiomeshP1 showed a significantly higher fibroblast proliferation around the nodes of the mesh compared to the straight filaments. On the NK1 mesh fibroblasts exclusively proliferated on the filaments but not on the pressed mesh surface. Conclusions. The polymer surface and structure appears to be of major importance for the biocompatibility of meshes: human fibroblasts preferably grow on low-weight meshes, thin filaments, and mesh nodes. Heavyweight meshes induce degenerative cell reactions. Polyglactin seems to further improve cell proliferation whereas a pressed mesh surface without pores hinders fibroblast growth."],["dc.identifier.doi","10.1007/s00104-005-1036-8"],["dc.identifier.isi","000232712300008"],["dc.identifier.pmid","15905969"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49910"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0009-4722"],["dc.title","In-vitro study of the cellular response of human fibroblasts cultured on alloplastic hernia meshes. Influence of mesh material and structure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","285"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","International Journal of Radiation Biology"],["dc.bibliographiccitation.lastpage","298"],["dc.bibliographiccitation.volume","84"],["dc.contributor.author","Koenig, Sarah"],["dc.contributor.author","Krause, Petra"],["dc.contributor.author","Schmidt, Thordis-Karen"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Rothe, Hilka"],["dc.contributor.author","Hermann, Robert Michael"],["dc.contributor.author","Becker, Heinz"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Christiansen, Hans"],["dc.date.accessioned","2018-11-07T11:20:07Z"],["dc.date.available","2018-11-07T11:20:07Z"],["dc.date.issued","2008"],["dc.description.abstract","Purpose: Hepatocyte transplantation following liver irradiation (IR) and partial hepatectomy (PH) leads to extensive liver repopulation. We investigated the changes in the liver induced by IR explaining the loss of reproductive integrity in endogenous hepatocytes. Materials and methods: Right lobules of rat liver underwent external beam IR (25 Gy). A second group was subjected to additional 33% PH of the untreated left liver lobule. Liver specimens and controls were analyzed for DNA damage, apoptosis, proliferation and cell cycle related genes (1 hour to up to 12 weeks). Results: Double strand breaks (phosphorylated histone H2AX) induced by IR rapidly declined within hours and were no longer detectable after 4 days. No significant apoptosis was noted and steady mRNA levels (B-cell lymphoma 2-associated X protein (BAX), caspase 3 and 9) were in line with the lack of DNA fragmentation. However, gene expression of p53 and p21 in irradiated liver tissue increased. Transcripts of cyclin D1, proliferating cell nuclear antigen (PCNA), and cyclin B augmented progressively, whereas cyclin E was only affected moderately. Following PH, irradiated livers displayed persistently high protein levels of p21 and cyclin D1. However, cell divisions were infrequent, as reflected by low PCNA levels up to four weeks. Conclusion: IR leads to a major arrest in the G1/S phase and to a lesser extent in the G2/M transition of the cell cycle, resulting in reduced regenerative response following PH. The persistent block of at least four weeks may promote preferential proliferation of transplanted hepatocytes in this milieu."],["dc.identifier.doi","10.1080/09553000801953359"],["dc.identifier.isi","000254631200004"],["dc.identifier.pmid","18386194"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55458"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Taylor & Francis Ltd"],["dc.relation.issn","1362-3095"],["dc.relation.issn","0955-3002"],["dc.title","Irradiation as preparative regimen for hepatocyte transplantation causes prolonged cell cycle block"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","220"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Nitric Oxide"],["dc.bibliographiccitation.lastpage","226"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Krause, Petra"],["dc.contributor.author","Waetzig, Esther"],["dc.contributor.author","Acil, Hasan"],["dc.contributor.author","Koenig, Sarah"],["dc.contributor.author","Unthan-Fechner, Kirsten"],["dc.contributor.author","Tsikas, Dimitrios"],["dc.contributor.author","Probst, Irmelin"],["dc.date.accessioned","2018-11-07T08:37:45Z"],["dc.date.available","2018-11-07T08:37:45Z"],["dc.date.issued","2010"],["dc.description.abstract","During liver regeneration in vivo carbon monoxide (CO) and nitric oxide (NO) are supposed to play a significant role. We raise the question whether CO and NO are involved in the growth process of cultured hepatocytes. Rat hepatocytes were stimulated into proliferation, growth being estimated by DNA content, mRNA by quantitative RT-PCR, and inducible NO synthase (iNOS) activity by GC-MS. Dexamethasone proved obligatory for fast proliferation. It suppressed the spontaneous rise of iNOS-mRNA in cultures devoid of glucocorticoids, but did not counteract the rise in mRNA in actively dividing cultures. Expression of iNOS-mRNA and cell growth were further enhanced by LiCl (10 mM). NOS activity was completely suppressed by the iNOS-specific inhibitors N-(3-(aminomethyl)benzyl) acetamidine (1400 W,100 mu M) and L-N(6)-(1-iminoethyl)lysine (L-NIL, 500 mu M), however, without a decrease in hepatocyte growth. Proliferation was attenuated only by very high concentrations (>0.5 mM) of N-nitro-L-arginine methyl ester NAME) and asymmetric dimethylarginine (ADMA). Various NO donors (at 100 mu M) did not stimulate cell growth. The furoxan CAS 1609 stimulated growth, decreased iNOS-mRNA expression and transiently increased haem oxygenase-1 (HO-1)-mRNA without releasing considerable amounts of NO. 1H-[1,2,4]Oxadiazolo[4,3,-alpha]quinoxalin-1-one (ODQ) attenuated the action of CAS 1609. Proliferation was stimulated by Co-protoporphyrin and tricarbonyldichlororuthenium(II) dimer (CORM-2). We conclude that CAS 1609 triggers hepatocyte mitosis most likely via direct, NO-independent induction of HO-1 expression, pointing to CO as a growth-promoting signal in the proliferation cascade in cultured hepatocytes. (C) 2010 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.niox.2010.06.007"],["dc.identifier.isi","000281659600010"],["dc.identifier.pmid","20619352"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18610"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","1089-8603"],["dc.title","Role of carbon monoxide and nitric oxide in adult rat hepatocytes proliferating in vitro: Effects of CAS 1609"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Strahlentherapie und Onkologie"],["dc.bibliographiccitation.volume","185"],["dc.contributor.author","Christiansen, H."],["dc.contributor.author","Krause, Petra"],["dc.contributor.author","Yuan, Q."],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Wolff, Hendrik Andreas"],["dc.contributor.author","Kafert-Kasting, S."],["dc.contributor.author","Ott, M."],["dc.contributor.author","Meyburg, Jan P."],["dc.contributor.author","Koenig, S."],["dc.date.accessioned","2018-11-07T08:29:44Z"],["dc.date.available","2018-11-07T08:29:44Z"],["dc.date.issued","2009"],["dc.format.extent","144"],["dc.identifier.isi","000268225500376"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16726"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Urban & Vogel"],["dc.publisher.place","Munich"],["dc.relation.conference","15th Annual Conference of the Deutschen-Gesellschaft-fur-Radioonkologie"],["dc.relation.eventlocation","Bremen, GERMANY"],["dc.relation.issn","0179-7158"],["dc.title","Liver re-population after radiation and ischemia/reperfusion damage as a proliferation stimulus conditioning in the rat model"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]