ArticleWorld journal of gastroenterology2014
Osteopontin is an important mediator of alcoholic liver disease via hepatic stellate cell activation.
Article in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 48 citations in OpenAlex.
- VCAM-1 and Osteopontin Link Hemodynamic Alteration to Fibrosis in Portal Hypertension.Cellular and molecular gastroenterology and hepatology · 2026Article
- Osteopontin: a central hub in the pathogenesis and therapeutic intervention of liver disease.Annals of medicine · 2025Review
- Hepatic Extracellular Matrix and Its Role in the Regulation of Liver Phenotype.Seminars in liver disease · 2024Review
- Advanced Biomarkers of Hepatotoxicity in Psychiatry: A Narrative Review and Recommendations for New Psychoactive Substances.International journal of molecular sciences · 2023Review
- Decoding liver fibrogenesis with single-cell technologies.Life medicine · 2022Review
- MyD88 in hepatic stellate cells promotes the development of alcoholic fatty liver via the AKT pathway.Journal of molecular medicine (Berlin, Germany) · 2022Article
- A Study on the Serum γ-Glutamyltranspeptidase and Plasma Osteopontin in Alcoholic Liver Disease.Journal of laboratory physicians · 2022Article
- Alcohol-Associated Tissue Injury: Current Views on Pathophysiological Mechanisms.Annual review of physiology · 2022Review
- Inflammatory Mechanisms Underlying Nonalcoholic Steatohepatitis and the Transition to Hepatocellular Carcinoma.Cancers · 2021Review
- Experimental models of metabolic and alcoholic fatty liver disease.World journal of gastroenterology · 2021Review
- Second hits exacerbate alcohol-related organ damage: an update.Alcohol and alcoholism (Oxford, Oxfordshire) · 2021Review
- Quantitative Expression of Key Cancer Markers in the AS-30D Hepatocarcinoma Model.Frontiers in oncology · 2021Article
- Osteopontin Expression Identifies a Subset of Recruited Macrophages Distinct from Kupffer Cells in the Fatty Liver.Immunity · 2020Article
- The Matrisome, Inflammation, and Liver Disease.Seminars in liver disease · 2020Review
- Immunomodulatory Role of the Extracellular Matrix Within the Liver Disease Microenvironment.Frontiers in immunology · 2020Review
- Aldehyde dehydrogenase-2 activation by Alda-1 decreases necrosis and fibrosis after bile duct ligation in mice.Free radical biology & medicine · 2019Article
- Pathogenesis, Early Diagnosis, and Therapeutic Management of Alcoholic Liver Disease.International journal of molecular sciences · 2019Review
- Role of mitochondrial depolarization and disrupted mitochondrial homeostasis in non-alcoholic steatohepatitis and fibrosis in mice.International journal of physiology, pathophysiology and pharmacology · 2019Article
- A Unifying Hypothesis Linking Hepatic Adaptations for Ethanol Metabolism to the Proinflammatory and Profibrotic Events of Alcoholic Liver Disease.Alcoholism, clinical and experimental research · 2018Review
- Hepatic expression profiling identifies steatosis-independent and steatosis-driven advanced fibrosis genes.JCI insight · 2018Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
aimTo investigate over-expression of Osteopontin (OPN) pathway expression and mechanisms of action in human alcoholic liver disease (ALD), in vivo and in vitro acute alcohol models.
methodsOPN pathway was evaluated in livers from patients with progressive stages of human ALD and serum from drinkers with and without liver cirrhosis. In vitro stellate LX2 cells exposed to acute alcohol and in vivo in acute alcoholic steatosis mouse models were also investigated for OPN pathway expression and function. WT and OPN(-/-) mice were administered an acute dose of alcohol and extent of liver injury was examined by histopathology and liver biochemistry after 16-24 h. The causative role of OPN was studied in OPN knockout animals and in vitro in stellate LX2 cells, utilizing siRNA, aptamer and neutralizing antibodies to block OPN and OPN pathway. OPN pathway expression and downstream functional consequences were measured for signaling by Western blotting, plasmin activation by spectrophotometric assays and cell migration by confocal imaging and quantitation.
resultsOPN expression positively correlated with disease severity in patients with progressive stages of ALD. In vivo, associated with alcoholic steatosis, a single dose of acute alcohol significantly increased hepatic OPN mRNA and protein, and a cleaved OPN form in a dose dependent manner. OPN mRNA and secreted OPN also increased in parallel with activation of LX2 stellate cells within 4 h of a single dose of alcohol. Expression of OPN receptors, αvβ3-integrin and CD44, increased in human ALD, and in vivo and in vitro with alcohol administration. This was accompanied by downstream phosphorylation of Akt and Erk, increased mRNA expression of several fibrogenesis, fibrinolysis and extracellular matrix pathway genes, plasmin activation and hepatic stellate cell (HSC) migration. Inhibition of OPN and OPN-receptor mediated signaling partially inhibited alcohol-induced HSC activation, plasmin activity and cell migration.
conclusionOPN is a key mediator of the alcohol-induced effects on hepatic stellate cell functions and liver fibrogenesis.
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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.