0000000000064645

AUTHOR

Johannes G. Bode

showing 2 related works from this author

Model Based Targeting of IL-6-Induced Inflammatory Responses in Cultured Primary Hepatocytes to Improve Application of the JAK Inhibitor Ruxolitinib

2017

IL-6 is a central mediator of the immediate induction of hepatic acute phase proteins (APP) in the liver during infection and after injury, but increased IL-6 activity has been associated with multiple pathological conditions. In hepatocytes, IL-6 activates JAK1-STAT3 signaling that induces the negative feedback regulator SOCS3 and expression of APPs. While different inhibitors of IL-6-induced JAK1-STAT3-signaling have been developed, understanding their precise impact on signaling dynamics requires a systems biology approach. Here we present a mathematical model of IL-6-induced JAK1-STAT3 signaling that quantitatively links physiological IL-6 concentrations to the dynamics of IL-6-induced …

0301 basic medicineRuxolitinibruxolitinibPhysiologySystems biologyRegulatorBiologyPharmacology: Biochemistry biophysics & molecular biology [F05] [Life sciences]lcsh:Physiology03 medical and health sciencesMediatoracute phase responsePhysiology (medical)medicineSOCS3primary hepatocytes: Biochimie biophysique & biologie moléculaire [F05] [Sciences du vivant]Original ResearchIL-6lcsh:QP1-981Acute-phase proteinmathematical modelingJAK-STAT signaling pathwayCell biology030104 developmental biologySignal transductionmedicine.drugFrontiers in Physiology
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Recent advances in 2D and 3D in vitro systems using primary hepatocytes, alternative hepatocyte sources and non-parenchymal liver cells and their use…

2013

This review encompasses the most important advances in liver functions and hepatotoxicity and analyzes which mechanisms can be studied in vitro. In a complex architecture of nested, zonated lobules, the liver consists of approximately 80 % hepatocytes and 20 % non-parenchymal cells, the latter being involved in a secondary phase that may dramatically aggravate the initial damage. Hepatotoxicity, as well as hepatic metabolism, is controlled by a set of nuclear receptors (including PXR, CAR, HNF-4α, FXR, LXR, SHP, VDR and PPAR) and signaling pathways. When isolating liver cells, some pathways are activated, e.g., the RAS/MEK/ERK pathway, whereas others are silenced (e.g. HNF-4α), resulting in…

MAPK/ERK pathwayHealth Toxicology and MutagenesisNF-KAPPA-BReceptors Cytoplasmic and NuclearReview ArticlePharmacologyToxicologyToxicogeneticsNon-parenchymal cells0302 clinical medicineInduced pluripotent stem cellANION-TRANSPORTING POLYPEPTIDECONSTITUTIVE ANDROSTANE RECEPTOR0303 health sciencesGeneral Medicine3. Good healthCell biologymedicine.anatomical_structureLiver030220 oncology & carcinogenesisHepatocyte[SDV.TOX]Life Sciences [q-bio]/ToxicologyInactivation MetabolicClearanceDILIStem cellPLURIPOTENT STEM-CELLSFARNESOID-X-RECEPTORSignal TransductionMechanisms of gene regulationARYL-HYDROCARBON RECEPTORCell signalingPharmacology and ToxicologyHEPATIC STELLATE CELLSBiology03 medical and health sciencesOrgan Culture TechniquesIn vivoCulture TechniquesToxicity TestsmedicineMathematical modeling.AnimalsHumansLiver X receptorDRUG-DRUG INTERACTIONS030304 developmental biologyCryopreservation[INFO.INFO-MO]Computer Science [cs]/Modeling and Simulation3D ModelsCoculture TechniquesHigh-Throughput Screening AssaysSALT EXPORT PUMPGene Expression RegulationHepatic stellate cellHepatocytes[SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologyPRIMARY RAT HEPATOCYTESMathematical modeling
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