ArticleGlia2008
Gene expression profiling of astrocytes from hyperammonemic mice reveals altered pathways for water and potassium homeostasis in vivo.
Article in Glia, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
39 citing papers in PubMed, 84 citations in OpenAlex.
- Current Treatment Modalities for Urea Cycle Disorders.Paediatric drugs · 2025Review
- Role of aquaporins in brain water transport and edema.Frontiers in neuroscience · 2025Review
- Unraveling the Link: Seizure Characteristics and Ammonia Levels in Urea Cycle Disorder During Hyperammonemic Crises.Pediatric neurology · 2024Observational
- Review
- Honey, I shrunk the extracellular space: Measurements and mechanisms of astrocyte swelling.Glia · 2022Review
- Acute Acquired Metabolic Encephalopathy Based on Diffusion MRI.Korean journal of radiology · 2021Review
- Article
- Imaging tripartite synapses using super-resolution microscopy.Methods (San Diego, Calif.) · 2020Article
- Silencing of Transcription Factor Sp1 Promotes SN1 Transporter Regulation by Ammonia in Mouse Cortical Astrocytes.International journal of molecular sciences · 2019Article
- Interstitial ion homeostasis and acid-base balance are maintained in oedematous brain of mice with acute toxic liver failure.Neurochemistry international · 2018Article
- Hyperammonemia in Hepatic Encephalopathy.Journal of clinical and experimental hepatology · 2018Review
- Combined Use of Emodin and Ginsenoside Rb1 Exerts Synergistic Neuroprotection in Cerebral Ischemia/Reperfusion Rats.Frontiers in pharmacology · 2018Article
- Diversity of astroglial responses across human neurodegenerative disorders and brain aging.Brain pathology (Zurich, Switzerland) · 2017Article
- Ammonia toxicity: from head to toe?Metabolic brain disease · 2017Review
- Gap Junction Intercellular Communication Mediates Ammonia-Induced Neurotoxicity.Neurotoxicity research · 2016Article
- Ammonia as a Potential Neurotoxic Factor in Alzheimer's Disease.Frontiers in molecular neuroscience · 2016Review
- Central Role of Maladapted Astrocytic Plasticity in Ischemic Brain Edema Formation.Frontiers in cellular neuroscience · 2016Review
- In Vivo NMR Studies of the Brain with Hereditary or Acquired Metabolic Disorders.Neurochemical research · 2015Review
- The central role of aquaporins in the pathophysiology of ischemic stroke.Frontiers in cellular neuroscience · 2015Review
- Heterogeneity of reactive astrocytes.Neuroscience letters · 2014Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Acute hyperammonemia (HA) causes cerebral edema and brain damage in children with urea cycle disorders (UCDs) and in patients in acute liver failure. Chronic HA is associated with developmental delay and mental retardation in children with UCDs, and with neuropsychiatric symptoms in patients with chronic liver failure. Astrocytes are a major cellular target of hyperammonemic encephalopathy, and changes occurring in these cells are thought to be causally related to the brain edema of acute HA. To study the effect of HA on astrocytes in vivo, we crossed the Otc(spf) mouse, a mouse with the X-linked UCD ornithine transcarbamylase (OTC) deficiency, with the hGFAP-EGFP mouse, a mouse selectively expressing green fluorescent protein in astrocytes. We used FACS to purify astrocytes from the brains of hyperammonemic and healthy Otcspf/GFAP-EGFP mice. RNA isolated from these astrocytes was used in microarray expression analyses and qRT-PCR. When compared with healthy littermates, we observed a significant downregulation of the gap-junction channel connexin 43 (Cx43) the water channel aquaporin 4 (Aqp4) genes, and the astrocytic inward-rectifying potassium channel (Kir) genes Kir4.1 and Kir5.1 in hyperammonemic mice. Aqp4, Cx43, and Kir4.1/Kir5.1 are co-localized to astrocytic end-feet at the brain vasculature, where they regulate potassium and water transport. Since, NH4+ ions can permeate water and K+-channels, downregulation of these three channels may be a direct effect of elevated blood ammonia levels. Our results suggest that alterations in astrocyte-mediated water and potassium homeostasis in brain may be key to the development of the brain edema.
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What OpenQuestion holds
Registered trials
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.