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10.1089/jir.2014.0096 http://scihub22266oqcxt.onion/10.1089/jir.2014.0096 C4490747!4490747 !25715168     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25715168 &cmd=llinks): Failed to open stream: HTTP request failed! 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Interferon-? Mediates Signaling Pathways Uniquely Regulated in Hepatic Stellate Cells and Attenuates the Progression of Hepatic Fibrosis in a Dietary Mouse Model |pdf=|usr=}}{{25715168 }} gab.com Text Interferon- Mediates Signaling Pathways Uniquely Regulated in Hepatic Stellate Cells and Attenuates the Progression of Hepatic Fibrosis in a Dietary Mouse Model JO: J Interferon Cytokine Res http://www.kidney.de/pget.php?&tw=1&pmid=25715168 #FOAvip The results of clinical and experimental studies suggest that type I interferons (IFNs) may have direct antifibrotic activity in addition to their antiviral properties. However, the mechanisms are still unclear; in particular, little is known about the antifibrotic activity of IFN-? and how its activity is distinct from that of IFN-?. Using DNA microarrays, we demonstrated that gene expression in TWNT-4 cells, an activated human hepatic stellate cell line, was remarkably altered by IFN-? more than by IFN-?. Integrated pathway enrichment analyses revealed that a variety of IFN-?-mediated signaling pathways are uniquely regulated in TWNT-4 cells, including those related to cell cycle and Toll-like receptor 4 (TLR4) signaling. To investigate the antifibrotic activity of IFN-? and the involvement of TLR4 signaling in vivo, we used mice fed a choline-deficient l-amino acid-defined diet as a model of nonalcoholic steatohepatitis-related hepatic fibrosis. In this model, the administration of IFN-? significantly attenuated augmentation of the area of liver fibrosis, with accompanying transcriptional downregulation of the TLR4 adaptor molecule MyD88. Our results provide important clues for understanding the mechanisms of the preferential antifibrotic activity of IFN-? and suggest that IFN-? itself, as well as being a modulator of its unique signaling pathway, may be a potential treatment for patients with hepatic fibrosis in a pathogenesis-independent manner. Twit Text FOAVip Interferon- Mediates Signaling Pathways Uniquely Regulated in Hepatic Stellate Cells and Attenuates the Progression of Hepatic Fibrosis in a Dietary Mouse Model ????J Interferon Cytokine Res http://www.kidney.de/pget.php?&tw=1&pmid=25715168 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25715168 #FOAvip English Wikipedia <ref>{{Cite pmid|25715168 }}</ref> Interferon-? Mediates Signaling Pathways Uniquely Regulated in Hepatic Stellate Cells and Attenuates the Progression of Hepatic Fibrosis in a Dietary Mouse Model #MMPMID25715168 Shimozono R ; Nishimura K ; Akiyama H ; Funamoto S ; Izawa A ; Sai T ; Kunita K ; Kainoh M ; Suzuki T ; Kawada N J Interferon Cytokine Res 2015[Jun]; 35 (6 ): 464-73 PMID25715168 show ga The results of clinical and experimental studies suggest that type I interferons (IFNs) may have direct antifibrotic activity in addition to their antiviral properties. However, the mechanisms are still unclear; in particular, little is known about the antifibrotic activity of IFN-? and how its activity is distinct from that of IFN-?. Using DNA microarrays, we demonstrated that gene expression in TWNT-4 cells, an activated human hepatic stellate cell line, was remarkably altered by IFN-? more than by IFN-?. Integrated pathway enrichment analyses revealed that a variety of IFN-?-mediated signaling pathways are uniquely regulated in TWNT-4 cells, including those related to cell cycle and Toll-like receptor 4 (TLR4) signaling. To investigate the antifibrotic activity of IFN-? and the involvement of TLR4 signaling in vivo, we used mice fed a choline-deficient l-amino acid-defined diet as a model of nonalcoholic steatohepatitis-related hepatic fibrosis. In this model, the administration of IFN-? significantly attenuated augmentation of the area of liver fibrosis, with accompanying transcriptional downregulation of the TLR4 adaptor molecule MyD88. Our results provide important clues for understanding the mechanisms of the preferential antifibrotic activity of IFN-? and suggest that IFN-? itself, as well as being a modulator of its unique signaling pathway, may be a potential treatment for patients with hepatic fibrosis in a pathogenesis-independent manner. |Animals [MESH] |Cell Cycle/drug effects [MESH] |Choline Deficiency/*drug therapy/metabolism/pathology [MESH] |Choline/metabolism [MESH] |Disease Models, Animal [MESH] |Disease Progression [MESH] |Food, Formulated [MESH] |Gene Expression Regulation [MESH] |Hepatic Stellate Cells/drug effects/metabolism/pathology [MESH] |Humans [MESH] |Interferon-alpha/metabolism/pharmacology [MESH] |Interferon-beta/metabolism/*pharmacology [MESH] |Liver Cirrhosis/*drug therapy/etiology/metabolism/pathology [MESH] |Liver/*drug effects/metabolism/pathology [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Myeloid Differentiation Factor 88/*genetics/metabolism [MESH] |Oligonucleotide Array Sequence Analysis [MESH] |Signal Transduction [MESH]Interferon-? Mediates Signaling Pathways Uniquely Regulated in Hepatic(epmc).pdf DeepDyve Pubget Overpricing