ArticleCell death & disease2014
Osteopontin deficiency aggravates hepatic injury induced by ischemia-reperfusion in mice.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Effects of iNOS in Hepatic Warm Ischaemia and Reperfusion Models in Mice and Rats: A Systematic Review and Meta-Analysis.International journal of molecular sciences · 2022Pooled it
- Article
- Reference Gene Validation for Quantitative PCR Analysis in 2D and 3D AML12 Hepatocyte Models.Biomedicines · 2026Article
- Osteopontin protects from ovalbumin-induced asthma by preserving the microbiome and the intestinal barrier function.mSystems · 2025Article
- Perfusate Liver Arginase 1 Levels After End-Ischemic Machine Perfusion Are Associated with Early Allograft Dysfunction.Biomedicines · 2025Article
- Emerging therapeutic strategies targeting extracellular histones for critical and inflammatory diseases: an updated narrative review.Frontiers in immunology · 2024Review
- Macrophage-derived Osteopontin (SPP1) Protects From Nonalcoholic Steatohepatitis.Gastroenterology · 2023Article
- Spatial transcriptomics analysis of zone-dependent hepatic ischemia-reperfusion injury murine model.Communications biology · 2023Article
- L-Cysteine attenuates osteopontin-mediated neuroinflammation following hypoxia-ischemia insult in neonatal mice by inducing S-sulfhydration of Stat3.Acta pharmacologica Sinica · 2022Article
- Potential Transdiagnostic Lipid Mediators of Inflammatory Activity in Individuals With Serious Mental Illness.Frontiers in psychiatry · 2021Article
- Tumour dormancy in inflammatory microenvironment: A promising therapeutic strategy for cancer-related bone metastasis.Cellular and molecular life sciences : CMLS · 2020Review
- MCD diet-induced steatohepatitis generates a diurnal rhythm of associated biomarkers and worsens liver injury in Klf10 deficient mice.Scientific reports · 2020Article
- Secreted Phosphoprotein 1 Expression in Retinal Mononuclear Phagocytes Links Murine to Human Choroidal Neovascularization.Frontiers in cell and developmental biology · 2020Article
- Circulating osteopontin per tumor volume as a prognostic biomarker for resectable intrahepatic cholangiocarcinoma.Hepatobiliary surgery and nutrition · 2019Article
- The Differential Expression of Cide Family Members is Associated with Nafld Progression from Steatosis to Steatohepatitis.Scientific reports · 2019Article
- Osteopontin protects against lung injury caused by extracellular histones.Mucosal immunology · 2019Article
- Serum osteopontin is a predictor of prognosis for HBV-associated acute-on-chronic liver failure.Biomedical reports · 2018Article
- Regulation of Cellular Redox Signaling by Matricellular Proteins in Vascular Biology, Immunology, and Cancer.Antioxidants & redox signaling · 2017Article
- The Effect of Osteopontin on Microglia.BioMed research international · 2017Review
- Neutralization of Osteopontin Ameliorates Acute Lung Injury Induced by Intestinal Ischemia-Reperfusion.Shock (Augusta, Ga.) · 2016Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteopontin (OPN) is a multifunctional protein involved in hepatic steatosis, inflammation, fibrosis and cancer progression. However, its role in hepatic injury induced by ischemia-reperfusion (I-R) has not yet been investigated. We show here that hepatic warm ischemia for 45 min followed by reperfusion for 4 h induced the upregulation of the hepatic and systemic level of OPN in mice. Plasma aspartate aminotransferase and alanine aminotransferase levels were strongly increased in Opn(-/-) mice compared with wild-type (Wt) mice after I-R, and histological analysis of the liver revealed a significantly higher incidence of necrosis of hepatocytes. In addition, the expression levels of inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNFα), interleukin 6 (IL6) and interferon-γ were strongly upregulated in Opn(-/-) mice versus Wt mice after I-R. One explanation for these responses could be the vulnerability of the OPN-deficient hepatocyte. Indeed, the downregulation of OPN in primary and AML12 hepatocytes decreased cell viability in the basal state and sensitized AML12 hepatocytes to cell death induced by oxygen-glucose deprivation and TNFα. Further, the downregulation of OPN in AML12 hepatocytes caused a strong decrease in the expression of anti-apoptotic Bcl2 and in the ATP level. The hepatic expression of Bcl2 also decreased in Opn(-/-) mice versus Wt mice livers after I-R. Another explanation could be the regulation of the macrophage activity by OPN. In RAW macrophages, the downregulation of OPN enhanced iNOS expression in the basal state and sensitized macrophages to inflammatory signals, as evaluated by the upregulation of iNOS, TNFα and IL6 in response to lipopolysaccharide. In conclusion, OPN partially protects from hepatic injury and inflammation induced in this experimental model of liver I-R. This could be due to its ability to partially prevent death of hepatocytes and to limit the production of toxic iNOS-derived NO by macrophages.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.