ArticleNeurobiology of disease2014
Aquaporin-4 deletion in mice reduces encephalopathy and brain edema in experimental acute liver failure.
Article in Neurobiology of disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 48 citations in OpenAlex.
- Effects of imbalanced gut microbial on mice with type a hepatic encephalopathy through the gut-liver-brain axis.Metabolic brain disease · 2026Article
- Melatonin as a potential adjunct therapy for central nervous system lupus: evidence from the MRL/lpr mouse model.Precision clinical medicine · 2024Article
- Aquaporins: Gatekeepers of Fluid Dynamics in Traumatic Brain Injury.International journal of molecular sciences · 2024Review
- Article
- Robust coagulation activation and coagulopathy in mice with experimental acetaminophen-induced liver failure.Journal of thrombosis and haemostasis : JTH · 2023Article
- 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
- The neurogliovascular unit in hepatic encephalopathy.JHEP reports : innovation in hepatology · 2021Review
- Therapeutic Applications of Resveratrol in Hepatic Encephalopathy through Its Regulation of the Microbiota, Brain Edema, and Inflammation.Journal of clinical medicine · 2021Review
- Estrogen Attenuates Traumatic Brain Injury by Inhibiting the Activation of Microglia and Astrocyte-Mediated Neuroinflammatory Responses.Molecular neurobiology · 2021Article
- Targeting the WNK-SPAK/OSR1 Pathway and Cation-Chloride Cotransporters for the Therapy of Stroke.International journal of molecular sciences · 2021Review
- Role of serine protease inhibitor, ulinastatin, in rat model of hepatic encephalopathy: aquaporin 4 molecular targeting and therapeutic implication.Journal of physiology and biochemistry · 2020Article
- Ammonia-Induced Glial-Inflammaging.Molecular neurobiology · 2020Article
- Serum osmolality, cerebrospinal fluid specific gravity and overt hepatic encephalopathy severity in patients with liver failure.Liver international : official journal of the International Association for the Study of the Liver · 2020Article
- Cerebral edema and liver disease: Classic perspectives and contemporary hypotheses on mechanism.Neuroscience letters · 2020Review
- Hyperammonemia in Hepatic Encephalopathy.Journal of clinical and experimental hepatology · 2018Review
- Blood-Brain Barrier Permeability Is Exacerbated in Experimental Model of Hepatic Encephalopathy via MMP-9 Activation and Downregulation of Tight Junction Proteins.Molecular neurobiology · 2018Article
- Osmotic Shifts, Cerebral Edema, and Neurologic Deterioration in Severe Hepatic Encephalopathy.Critical care medicine · 2018Article
- Ammonia toxicity: from head to toe?Metabolic brain disease · 2017Review
- Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Brain edema and associated astrocyte swelling leading to increased intracranial pressure are hallmarks of acute liver failure (ALF). Elevated blood and brain levels of ammonia have been implicated in the development of brain edema in ALF. Cultured astrocytes treated with ammonia have been shown to undergo cell swelling and such swelling was associated with an increase in the plasma membrane expression of aquaporin-4 (AQP4) protein. Further, silencing the AQP4 gene in cultured astrocytes was shown to prevent the ammonia-induced cell swelling. Here, we examined the evolution of brain edema in AQP4-null mice and their wild type counterparts (WT-mice) in different models of ALF induced by thioacetamide (TAA) or acetaminophen (APAP). Induction of ALF with TAA or APAP significantly increased brain water content in WT mice (by 1.6% ± 0.3 and 2.3 ± 0.4%, respectively). AQP4 protein was significantly increased in brain plasma membranes of WT mice with ALF induced by either TAA or APAP. In contrast to WT-mice, brain water content did not increase in AQP4-null mice. Additionally, AQP4-null mice treated with either TAA or APAP showed a remarkably lesser degree of neurological deficits as compared to WT mice; the latter displayed an inability to maintain proper gait, and demonstrated a markedly reduced exploratory behavior, with the mice remaining in one corner of the cage with its head tilted downwards. These results support a central role of AQP4 in the brain edema associated with ALF.
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