ArticleBioMed research international2015
Lost Polarization of Aquaporin4 and Dystroglycan in the Core Lesion after Traumatic Brain Injury Suggests Functional Divergence in Evolution.
Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 22 citations in OpenAlex.
- Noradrenergic Slow Vasomotion: The Hidden Fluid Pump Linking Sleep, Brain Clearance, and Dementia Pathogenesis.International journal of molecular sciences · 2025Review
- Pathological changes and aquaporin-4 expression after bevacizumab treatment of traumatic penumbra in the rat brain.Scientific reports · 2025Article
- Knockdown of RUNX2 Attenuated A1 Astrocyte Overactivation, Brain Injury, and Cerebral Edema During Ischemic Stroke.Neuromolecular medicine · 2025Article
- Aquaporins in Acute Brain Injury: Insights from Clinical and Experimental Studies.Biomedicines · 2025Review
- Advances in understanding the pathogenesis of post-traumatic epilepsy: a literature review.Frontiers in neurology · 2023Review
- Article
- A Microfluidic Model of AQP4 Polarization Dynamics and Fluid Transport in the Healthy and Inflamed Human Brain: The First Step Towards Glymphatics-on-a-Chip.Advanced biology · 2022Article
- Association of Serum Dystroglycan, MMP-2/9 and AQP-4 with Haematoma Expansion in Patients with Intracerebral Haemorrhage.Neuropsychiatric disease and treatment · 2021Article
- No rapid and demarcating astroglial reaction to stab wounds in Agama and Gecko lizards and the caiman Paleosuchus - it is confined to birds and mammals.Histology and histopathology · 2020Article
- Glioma-Induced Alterations in Neuronal Activity and Neurovascular Coupling during Disease Progression.Cell reports · 2020Article
- Cerebral Edema in Traumatic Brain Injury: a Historical Framework for Current Therapy.Current treatment options in neurology · 2020Article
- Pathophysiology and treatment of cerebral edema in traumatic brain injury.Neuropharmacology · 2019Review
- A Precision Medicine Approach to Cerebral Edema and Intracranial Hypertension after Severe Traumatic Brain Injury: Quo Vadis?Current neurology and neuroscience reports · 2018Review
- Human and mouse cortical astrocytes differ in aquaporin-4 polarization toward microvessels.Glia · 2017Article
- Sex differences in astrocyte and microglia responses immediately following middle cerebral artery occlusion in adult mice.Neuroscience · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo understand how aquaporin4 (AQP4) and dystroglycan (DG) polarized distribution change and their roles in brain edema formation after traumatic brain injury (TBI).
methodsBrain water content, Evans blue detection, real-time PCR, western blot, and immunofluorescence were used.
resultsAt an early stage of TBI, AQP4 and DG maintained vessel-like pattern in perivascular endfeet; M1, M23, and M1/M23 were increased in the core lesion. At a later stage of TBI, DG expression was lost in perivascular area, accompanied with similar but delayed change of AQP4 expression; expression of M1, M23, and DG and the ratio of M1/M2 were increased.
conclusionAt an early stage, AQP4 and DG maintained the polarized distribution. Upregulated M1 and M23 could retard the cytotoxic edema formation. At a later stage AQP4 and DG polarized expression were lost from perivascular endfeet and induced the worst cytotoxic brain edema. The alteration of DG expression could regulate that of AQP4 expression after TBI.
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.