ArticlePloS one2014
Altered astrocytic swelling in the cortex of α-syntrophin-negative GFAP/EGFP mice.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- Pathophysiological Role of Perivascular Macrophages in Blood-Brain Barrier Dysfunction Induced by Cerebral Hypoperfusion in Mice.Neurochemical research · 2026Article
- The deletion of AQP4 and TRPV4 affects astrocyte swelling/volume recovery in response to ischemia-mimicking pathologies.Frontiers in cellular neuroscience · 2024Article
- Pathophysiology, Management, and Therapeutics in Subarachnoid Hemorrhage and Delayed Cerebral Ischemia: An Overview.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023Review
- A view of the genetic and proteomic profile of extracellular matrix molecules in aging and stroke.Frontiers in cellular neuroscience · 2023Article
- Entopallium Lost GFAP Immunoreactivity during Avian Evolution: Is GFAP a "Condition Sine Qua Non"?Brain, behavior and evolution · 2023Article
- The absence of AQP4/TRPV4 complex substantially reduces acute cytotoxic edema following ischemic injury.Frontiers in cellular neuroscience · 2022Article
- Compromised Astrocyte Swelling/Volume Regulation in the Hippocampus of the Triple Transgenic Mouse Model of Alzheimer's Disease.Frontiers in aging neuroscience · 2021Article
- The Glymphatic System: A Novel Therapeutic Target for Stroke Treatment.Frontiers in aging neuroscience · 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
- Multifaceted roles of pericytes in central nervous system homeostasis and disease.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020Review
- Genetic underpinnings of cerebral edema in acute brain injury: an opportunity for pathway discovery.Neuroscience letters · 2020Review
- The Effect of Hapln4 Link Protein Deficiency on Extracellular Space Diffusion Parameters and Perineuronal Nets in the Auditory System During Aging.Neurochemical research · 2020Article
- Distribution of GFAP in Squamata: Extended Immunonegative Areas, Astrocytes, High Diversity, and Their Bearing on Evolution.Frontiers in neuroanatomy · 2020Article
- Bursting at the Seams: Molecular Mechanisms Mediating Astrocyte Swelling.International journal of molecular sciences · 2019Review
- Exploring the Role of Astroglial Glutamate Release and Association With Synapses in Neuronal Function and Behavior.Biological psychiatry · 2018Review
- Astroglial Modulation of Hydromineral Balance and Cerebral Edema.Frontiers in molecular neuroscience · 2018Review
- Turning down the volume: Astrocyte volume change in the generation and termination of epileptic seizures.Neurobiology of disease · 2017Review
- Article
- Hippocampal and Cortical Pyramidal Neurons Swell in Parallel with Astrocytes during Acute Hypoosmolar Stress.Frontiers in cellular neuroscience · 2017Article
- Brain edema: a valid endpoint for measuring hepatic encephalopathy?Metabolic brain disease · 2016Review
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain edema accompanying ischemic or traumatic brain injuries, originates from a disruption of ionic/neurotransmitter homeostasis that leads to accumulation of K(+) and glutamate in the extracellular space. Their increased uptake, predominantly provided by astrocytes, is associated with water influx via aquaporin-4 (AQP4). As the removal of perivascular AQP4 via the deletion of α-syntrophin was shown to delay edema formation and K(+) clearance, we aimed to elucidate the impact of α-syntrophin knockout on volume changes in individual astrocytes in situ evoked by pathological stimuli using three dimensional confocal morphometry and changes in the extracellular space volume fraction (α) in situ and in vivo in the mouse cortex employing the real-time iontophoretic method. RT-qPCR profiling was used to reveal possible differences in the expression of ion channels/transporters that participate in maintaining ionic/neurotransmitter homeostasis. To visualize individual astrocytes in mice lacking α-syntrophin we crossbred GFAP/EGFP mice, in which the astrocytes are labeled by the enhanced green fluorescent protein under the human glial fibrillary acidic protein promoter, with α-syntrophin knockout mice. Three-dimensional confocal morphometry revealed that α-syntrophin deletion results in significantly smaller astrocyte swelling when induced by severe hypoosmotic stress, oxygen glucose deprivation (OGD) or 50 mM K(+). As for the mild stimuli, such as mild hypoosmotic or hyperosmotic stress or 10 mM K(+), α-syntrophin deletion had no effect on astrocyte swelling. Similarly, evaluation of relative α changes showed a significantly smaller decrease in α-syntrophin knockout mice only during severe pathological conditions, but not during mild stimuli. In summary, the deletion of α-syntrophin markedly alters astrocyte swelling during severe hypoosmotic stress, OGD or high K(+).
Indexed as
Identifiers
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.