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  • 1
    Keywords: RECEPTOR ; EXPRESSION ; GROWTH ; CELL ; Germany ; liver ; GENE ; GENE-EXPRESSION ; microarray ; transcription ; DIFFERENTIATION ; MOLECULES ; DNA ; TRANSCRIPTION FACTOR ; DOMAIN ; hepatocytes ; BINDING ; BIOLOGY ; MOLECULE ; MATURATION ; MOUSE ; TRANSCRIPTION FACTORS ; gene expression ; MUTATION ; genetics ; DNA-BINDING ; MUTATIONS ; glucocorticoid receptor ; BODY ; GLUCOCORTICOID-RECEPTOR ; REPRESSION ; heredity ; CROSS-TALK ; BODIES ; RE ; BODY-SIZE ; interaction ; ACTIVATOR ; SIGNAL TRANSDUCER ; GROWTH-FACTOR-I ; SIZE ; USA ; STAT5 ; SET ; BONE-GROWTH ; Cre-loxP ; growth hormone ; LYMPHOID DEVELOPMENT ; somatomedin
    Abstract: The glucocorticoid receptor regulates transcription through DNA binding as well as through cross-talk with other transcription factors. In hepatocytes, the glucocorticoid receptor is critical for normal postnatal growth. Using hepatocyte- specific and domain-selective mutations in the mouse we show that Stat5 in hepatocytes is essential for normal postnatal growth and that it mediates the growth- promoting effect of the glucocorticoid receptor through a direct interaction involving the N-terminal tetramerization domain of Stat5b. This interaction mediates a selective and unexpectedly extensive part of the transcriptional actions of these molecules since it controls the expression of gene sets involved in growth and sexual maturation
    Type of Publication: Journal article published
    PubMed ID: 17504935
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  • 2
    Keywords: RECEPTOR ; EXPRESSION ; GROWTH ; GROWTH-FACTOR ; proliferation ; tumor ; FACTOR RECEPTOR ; INHIBITION ; MODEL ; PATHWAY ; PATHWAYS ; DISEASE ; liver ; GENE ; GENES ; transcription ; MICE ; TUMOR-NECROSIS-FACTOR ; DOWN-REGULATION ; GROWTH-FACTOR RECEPTOR ; ALPHA ; ACID ; MOUSE ; resistance ; INDUCED APOPTOSIS ; UP-REGULATION ; NECROSIS-FACTOR-ALPHA ; inactivation ; DAMAGE ; SIGNALING PATHWAY ; SIGNALING PATHWAYS ; PHENOTYPE ; MOUSE MODEL ; INJURY ; EPIDERMAL-GROWTH-FACTOR ; INCREASED EXPRESSION ; signaling ; CYTOKINE ; FAS ; BILE ; INTERLEUKIN-6 ; KNOCKOUT MICE ; methods ; BARRIER ; NECROSIS ; Stat3 ; CHOLESTASIS ; interleukin 6 ; FACTOR-RECEPTOR ; Conditional mouse model ; BILE-ACIDS ; PRIMARY HEPATOCYTES
    Abstract: BACKGROUND & AIMS: Signal transducer and activator of transcription 3 (Stat3) is the main mediator of interleukin-6-type cytokine signaling required for hepatocyte proliferation and hepatoprotection, but its role in sclerosing cholangitis and other cholestatic liver diseases remains unresolved. METHODS: We investigated the role of Stat3 in inflammation-induced cholestatic liver injury and used mice lacking the multidrug resistance gene 2 (mdr2(-/-)) as a model for SC. RESULTS: We show that conditional inactivation of Stat3 in hepatocytes and cholangiocytes (stat3(Delta hc)) of mdr2(-/-) mice strongly aggravated bile acid-induced liver injury and fibrosis. A similar phenotype was observed in mdr2(-/-) mice lacking interleukin-6 production. Biochemical and molecular characterization suggested that Stat3 exerts hepatoprotective functions in both hepatocytes and cholangiocytes. Loss of Stat3 led to increased expression of tumor necrosis factor alpha, which might reduce the barrier function of bile ducts. Moreover, Stat3-deficient hepatocytes displayed up-regulation of bile acid biosynthesis genes and down-regulation of hepatoprotective epidermal growth factor receptor and insulin-like growth factor 1 signaling pathways. Consistently, stat3(Delta hc) mice were more sensitive to cholic acid-induced liver damage than control mice. CONCLUSIONS: Our data suggest that Stat3 prevents cholestasis and liver damage in sclerosing cholangitis via regulation of pivotal functions in hepatocytes and cholangiocytes
    Type of Publication: Journal article published
    PubMed ID: 20193684
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