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10.1038/srep11231 http://scihub22266oqcxt.onion/10.1038/srep11231 C4466889!4466889 !26073647     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26073647 &cmd=llinks): Failed to open stream: HTTP request failed! 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Aggravation of post-ischemic liver injury by overexpression of insulin-like growth factor binding protein 3 |pdf=|usr=}}{{26073647 }} gab.com Text Aggravation of post-ischemic liver injury by overexpression of insulin-like growth factor binding protein 3 JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26073647 #FOAvip Insulin-like growth factor-1 (IGF-1) is known to inhibit reperfusion-induced apoptosis. IGF-binding protein-3 (IGFBP-3) is the major circulating carrier protein for IGF-1 and induces apoptosis. In this study, we determined if IGFBP-3 was important in the hepatic response to I/R. To deliver IGFBP-3, we used an adenovirus containing IGFBP-3 cDNA (AdIGFBP-3) or an IGFBP-3 mutant devoid of IGF binding affinity but retaining IGFBP-3 receptor binding ability (AdIGFBP-3(GGG)). Mice subjected to I/R injury showed typical patterns of hepatocellular damage. Protein levels of IGFBP-3 were increased after reperfusion and showed a positive correlation with the extent of liver injury. Prior injection with AdIGFBP-3 aggravated liver injury: serum aminotransferases, prothrombin time, proinflammatory cytokines, hepatocellular necrosis and apoptosis, and neutrophil infiltration were markedly increased compared to control mice. A decrease in antioxidant potential and an upregulation of NADPH oxidase might have caused these aggravating effects of IGFBP-3. Experiments using HepG2 cells and N-acetylcysteine-pretreated mice showed a discernible effect of IGFBP-3 on reactive oxygen species generation. Lastly, AdIGFBP-3 abolished the beneficial effects of ischemic preconditioning and hypothermia. Mice treated with AdIGFBP-3(GGG) exhibited effects similar to those of AdIGFBP-3, suggesting a ligand-independent effect of IGFBP-3. Our results suggest IGFBP-3 as an aggravating factor during hepatic I/R injury. Twit Text FOAVip Aggravation of post-ischemic liver injury by overexpression of insulin-like growth factor binding protein 3 ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26073647 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26073647 #FOAvip English Wikipedia <ref>{{Cite pmid|26073647 }}</ref> Aggravation of post-ischemic liver injury by overexpression of insulin-like growth factor binding protein 3 #MMPMID26073647 Zhou L ; Koh HW ; Bae UJ ; Park BH Sci Rep 2015[Jun]; 5 (ä): 11231 PMID26073647 show ga Insulin-like growth factor-1 (IGF-1) is known to inhibit reperfusion-induced apoptosis. IGF-binding protein-3 (IGFBP-3) is the major circulating carrier protein for IGF-1 and induces apoptosis. In this study, we determined if IGFBP-3 was important in the hepatic response to I/R. To deliver IGFBP-3, we used an adenovirus containing IGFBP-3 cDNA (AdIGFBP-3) or an IGFBP-3 mutant devoid of IGF binding affinity but retaining IGFBP-3 receptor binding ability (AdIGFBP-3(GGG)). Mice subjected to I/R injury showed typical patterns of hepatocellular damage. Protein levels of IGFBP-3 were increased after reperfusion and showed a positive correlation with the extent of liver injury. Prior injection with AdIGFBP-3 aggravated liver injury: serum aminotransferases, prothrombin time, proinflammatory cytokines, hepatocellular necrosis and apoptosis, and neutrophil infiltration were markedly increased compared to control mice. A decrease in antioxidant potential and an upregulation of NADPH oxidase might have caused these aggravating effects of IGFBP-3. Experiments using HepG2 cells and N-acetylcysteine-pretreated mice showed a discernible effect of IGFBP-3 on reactive oxygen species generation. Lastly, AdIGFBP-3 abolished the beneficial effects of ischemic preconditioning and hypothermia. Mice treated with AdIGFBP-3(GGG) exhibited effects similar to those of AdIGFBP-3, suggesting a ligand-independent effect of IGFBP-3. Our results suggest IGFBP-3 as an aggravating factor during hepatic I/R injury. |Acetylcysteine/pharmacology [MESH] |Adenoviridae/genetics [MESH] |Alanine Transaminase/blood [MESH] |Animals [MESH] |Apoptosis/genetics [MESH] |Aspartate Aminotransferases/blood [MESH] |Free Radical Scavengers/pharmacology [MESH] |Gene Expression Regulation [MESH] |Genetic Vectors [MESH] |Hep G2 Cells [MESH] |Humans [MESH] |Hypothermia, Induced [MESH] |Insulin-Like Growth Factor Binding Protein 3/*genetics/metabolism [MESH] |Insulin-Like Growth Factor I/*genetics/metabolism [MESH] |Ischemic Preconditioning [MESH] |Liver/*metabolism/pathology [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Necrosis/genetics/*metabolism/pathology/prevention & control [MESH] |Neutrophil Infiltration/drug effects [MESH] |Reactive Oxygen Species/metabolism [MESH] |Reperfusion Injury/*genetics/metabolism/pathology/prevention & control [MESH] |Signal Transduction [MESH]Aggravation of post-ischemic liver injury by overexpression of insulin(epmc).pdf DeepDyve Pubget Overpricing