DC Field | Value | Language |
---|---|---|
dc.contributor.author | Zhou, Lu | ko |
dc.contributor.author | Koh, Hyoung-Won | ko |
dc.contributor.author | Bae, Ui-Jin | ko |
dc.contributor.author | Park, Byung-Hyun | ko |
dc.date.accessioned | 2024-03-22T07:01:26Z | - |
dc.date.available | 2024-03-22T07:01:26Z | - |
dc.date.created | 2024-03-21 | - |
dc.date.issued | 2015-06 | - |
dc.identifier.citation | SCIENTIFIC REPORTS, v.5 | - |
dc.identifier.issn | 2045-2322 | - |
dc.identifier.uri | http://hdl.handle.net/10203/318786 | - |
dc.description.abstract | 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. | - |
dc.language | English | - |
dc.publisher | NATURE PORTFOLIO | - |
dc.title | Aggravation of post-ischemic liver injury by overexpression of insulin-like growth factor binding protein 3 | - |
dc.type | Article | - |
dc.identifier.wosid | 000356507500001 | - |
dc.identifier.scopusid | 2-s2.0-84931274887 | - |
dc.type.rims | ART | - |
dc.citation.volume | 5 | - |
dc.citation.publicationname | SCIENTIFIC REPORTS | - |
dc.identifier.doi | 10.1038/srep11231 | - |
dc.contributor.localauthor | Park, Byung-Hyun | - |
dc.contributor.nonIdAuthor | Zhou, Lu | - |
dc.contributor.nonIdAuthor | Koh, Hyoung-Won | - |
dc.contributor.nonIdAuthor | Bae, Ui-Jin | - |
dc.description.isOpenAccess | N | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordPlus | ISCHEMIA-REPERFUSION INJURY | - |
dc.subject.keywordPlus | HEPATIC ISCHEMIA/REPERFUSION INJURY | - |
dc.subject.keywordPlus | FACTOR-I PRODUCTION | - |
dc.subject.keywordPlus | KAPPA-B | - |
dc.subject.keywordPlus | REACTIVE OXYGEN | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | NADPH OXIDASE | - |
dc.subject.keywordPlus | RAT-LIVER | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | MECHANISMS | - |
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