ArticleScientific reports2015
Aggravation of post-ischemic liver injury by overexpression of insulin-like growth factor binding protein 3.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Review
- Knockout of IGFBP3 improves alcohol-induced liver injury via Akt/GSK3β and TMEM219/caspase 8 pathways.Frontiers in physiology · 2026Article
- Stage-specific role of IGFBP-3/TMEM219 pathway in liver fibrosis progression using a bile duct ligation rat model.Molecular biology reports · 2025Article
- Introducing critical proteins related to liver ischemia/reperfusion injury.Gastroenterology and hepatology from bed to bench · 2024Article
- Genetic Regulation of Liver Metabolites and Transcripts Linking to Biochemical-Clinical Parameters.Frontiers in genetics · 2019Article
- Sirtuin 2 aggravates postischemic liver injury by deacetylating mitogen-activated protein kinase phosphatase-1.Hepatology (Baltimore, Md.) · 2017Article
- The protein kinase 2 inhibitor tetrabromobenzotriazole protects against renal ischemia reperfusion injury.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
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