ArticleMetabolic brain disease2010
Brain expression of the water channels aquaporin-1 and -4 in mice with acute liver injury, hyperammonemia and brain edema.
Article in Metabolic brain disease, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 43 citations in OpenAlex.
- Inflammatory Factors Derived From Metabolic Dysfunction-Alcoholic Fatty Liver Disease: Inducers of Anxiety and Spatial Memory Impairment.Mediators of inflammation · 2026Article
- Hepatic encephalopathy as a result of ammonia-induced increase in GABAergic tone with secondary reduced brain energy metabolism.Metabolic brain disease · 2024Review
- Lessons on brain edema in HE: from cellular to animal models and clinical studies.Metabolic brain disease · 2024Review
- Connecting the Dots: The Cerebral Lymphatic System as a Bridge Between the Central Nervous System and Peripheral System in Health and Disease.Aging and disease · 2024Review
- Severe Acute Liver Dysfunction Induces Delayed Hepatocyte Swelling and Cytoplasmic Vacuolization, and Delayed Cortical Neuronal Cell Death.International journal of molecular sciences · 2023Article
- New Insight Into Mechanisms of Hepatic Encephalopathy: An Integrative Analysis Approach to Identify Molecular Markers and Therapeutic Targets.Bioinformatics and biology insights · 2023Article
- Severe Acute Hepatic Dysfunction Induced by Ammonium Acetate Treatment Results in Choroid Plexus Swelling and Ventricle Enlargement in the Brain.International journal of molecular sciences · 2022Article
- Ammonia induced microglia activation was associated with limited effects on connexin 43 and aquaporin 4 expression in an astrocyte-microglia co-culture model.BMC neuroscience · 2021Article
- Cerebral edema and liver disease: Classic perspectives and contemporary hypotheses on mechanism.Neuroscience letters · 2020Review
- The Direct Contribution of Astrocytes and Microglia to the Pathogenesis of Hepatic Encephalopathy.Journal of clinical and translational hepatology · 2019Review
- Lactulose decreases neuronal activation and attenuates motor behavioral deficits in hyperammonemic rats.Metabolic brain disease · 2017Article
- [Effect of different concentrations of ammonium chloride on expression of hypoxia-inducible factor-1α in Chang liver cells].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2016Article
- Potential role of Plasmodium falciparum-derived ammonia in the pathogenesis of cerebral malaria.Frontiers in neuroscience · 2015Article
- Brain edema in acute liver failure: mechanisms and concepts.Metabolic brain disease · 2014Review
- Aquaporin-4 deletion in mice reduces encephalopathy and brain edema in experimental acute liver failure.Neurobiology of disease · 2014Article
- Dexamethasone attenuates LPS-induced changes in expression of urea transporter and aquaporin proteins, ameliorating brain endotoxemia in mice.International journal of clinical and experimental pathology · 2014Article
- Molecular pathology of brain edema after severe burns in forensic autopsy cases with special regard to the importance of reference gene selection.International journal of legal medicine · 2013Article
- Transporters and channels in cytotoxic astrocyte swelling.Neurochemical research · 2012Review
- Blood-brain barrier in acute liver failure.Neurochemistry international · 2012Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral edema is a feared complication to acute liver failure (ALF), but the pathogenesis is still poorly understood. The water channels Aquaporin-1 (Aqp1) and -4 (Aqp4) has been associated with brain edema formation in several neuropathological conditions, indicating a possible role of Aqp1 and/or Aqp4 in ALF mediated brain edema. We induced acute liver injury and hyperammonemia in mice, to evaluate brain edema formation and the parallel expression of Aqp1 and Aqp4 in ALF. Liver injury and hyperammonemia were induced by +D-galactosamine (GLN) plus lipopolysaccharide (LPS) intraperitoneally and intravenous ammonia-acetate (NH(4)(+)), the GLN+LPS+NH(4)(+) group. The vehicle control group (CONTROL) was treated with NaCl and phosphate-buffered saline. The GLN+LPS+NH(4)(+) group showed significantly elevated p-alanine aminotransferase, p-INR and p-ammonium vs. CONTROL (p < 0.001). Cortical brain water content was significantly elevated in the GLN+LPS+NH(4)(+) group vs. CONTROL, mean (SEM) 80.8(0.3) vs 80.0(0.1) % (p < 0.05). Western blot of membrane enriched cortical brain tissue showed significantly upregulation of Aqp4 in the GLN+LPS+NH(4)(+) group vs. CONTROL, mean AU (SEM) 100775(14820) vs. 58857(6266) (p < 0.05), and stationary levels for Aqp1. Aqp1 and Aqp4 mRNA were stationary. This study indicates that Aqp4, but not Aqp1, may be of importance in the pathogenesis of cortical brain edema in mice with ALF.
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