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Download windows 98 plus themes for windows xp. The Activator Protein 1 (AP‐1) transcription factor subunit Fos‐related antigen 1 (Fra‐1) has been implicated in liver fibrosis. Here we used loss‐of‐function as well as switchable, cell type‐specific, gain‐of‐function alleles for Fra‐1 to investigate the relevance of Fra‐1 expression in cholestatic liver injury and fibrosis. Our results indicate that Fra‐1 is dispensable in three well‐established, complementary models of liver fibrosis. However, broad Fra‐1 expression in adult mice results in liver fibrosis, which is reversible, when ectopic Fra‐1 is switched off. Interestingly, hepatocyte‐specific Fra‐1 expression is not sufficient to trigger the disease, although Fra‐1 expression leads to dysregulation of fibrosis‐associated genes.

Both opn and cxcl9 are controlled by Fra‐1 in gain‐of‐function and loss‐of‐function experiments. Importantly, Fra‐1 attenuates liver damage in the 3,5‐diethoxycarbonyl‐1,4‐dihydrocollidine‐feeding cholestatic liver injury model. Strikingly, manipulating Fra‐1 expression affects genes involved in hepatic transport and detoxification, in particular glutathione S‐transferases. Molecular analyses indicate that Fra‐1 binds to the promoters of cxcl9 and gstp1 in vivo. Furthermore, loss of Fra‐1 sensitizes, while hepatic Fra‐1 expression protects from acetaminophen‐induced liver damage, a paradigm for glutathione‐mediated acute liver failure. Conclusion: These data define a novel function of Fra‐1/AP‐1 in modulating the expression of detoxification genes and the adaptive response of the liver to bile acids/xenobiotic overload. (H epatology 2014;58:261–273).

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The liver performs a wide range of functions including nutrient synthesis, transformation and storage, as well as endogenous and exogenous substance detoxification. Studies using genetically modified mice revealed essential functions of the dimeric transcription factor Activator Protein 1 (AP‐1) in controlling liver development, homeostasis, and disease. For example, c‐Jun is critical for hepatocyte proliferation and survival during liver development, regeneration, inflammation, and cancer. - Although the close homologs junb and jund are dispensable for liver homeostasis,, JunD‐deficient mice are sensitive to tumor necrosis factor alpha (TNF‐α)‐mediated hepatitis and protected from carbon tetrachloride (CCl 4)‐induced liver fibrosis. Furthermore, junb and jund can substitute for c‐jun during fetal liver development., In contrast, the functions of Fos proteins in liver physiology are less well defined.

C‐Fos, FosB, Fra‐1, and Fra‐2 form AP‐1 complexes by association with Jun proteins. Genetic inactivation of single fos genes has no obvious effect on liver homeostasis (reviewed ) and the relevance of Fos proteins to liver disease in loss‐of‐function mouse models has not been reported. Interestingly, broad ectopic expression of Fra‐1 or Fra‐2 in transgenic mice resulted in increased bone mass, but also generalized fibrosis with predominant manifestation in the liver and lung.

- In addition, Fra‐1 transgenic mice (Fra‐1 Tg) developed an inflammation‐associated ductular reaction preceding liver fibrosis, suggesting an involvement of Fra‐1 in cholestatic liver disease. Hepatic fibrosis is the final common endpoint of most chronic liver diseases. We set out to define the contribution of Fra‐1/AP‐1 to the pathogenesis of cholestasis and hepatic fibrosis using Fra‐1 loss‐of‐function mice and novel mouse models with switchable ectopic Fra‐1 alleles. Our results indicate that Fra‐1 is dispensable for liver fibrosis in three independent experimental models. However, broad Fra‐1 expression results in reversible periportal liver fibrosis affecting opn and cxcl9 expression in hepatocytes. Strikingly, these experiments revealed that Fra‐1 modulates the expression of genes involved in xenobiotic detoxification and that Fra‐1/AP‐1 is relevant for acetaminophen (APAP)‐induced liver failure.