ArticleThe Journal of biological chemistry2014
Sustained down-regulation of β-dystroglycan and associated dysfunctions of astrocytic endfeet in epileptic cerebral cortex.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- The Role of Aquaporins in Epileptogenesis-A Systematic Review.International journal of molecular sciences · 2023Pooled it
- β-Dystroglycan Downregulation and Astrocytic Alterations: A Possible Role in Blood-Brain Barrier Disruption During Experimental Cerebral Malaria.Molecular neurobiology · 2025Article
- Pharmacological inhibition of SPAK-NKCC1 complex attenuates astrogliosis and restores cerebral blood flow in a mouse model of VCID.Acta neuropathologica communications · 2025Article
- Teneurin-2 and related proteins in reactive astrocytes afterFrontiers in neuroscience · 2025Article
- Edaravone Maintains AQP4 Polarity Via OS/MMP9/β-DG Pathway in an Experimental Intracerebral Hemorrhage Mouse Model.Molecular neurobiology · 2024Article
- Matrix metalloproteinase-9 inhibition prevents aquaporin-4 depolarization-mediated glymphatic dysfunction in Parkinson's disease.Journal of advanced research · 2024Article
- The cell adhesion protein dystroglycan affects the structural remodeling of dendritic spines.Scientific reports · 2022Article
- Editorial: The role of astrocyte in vascular aging.Frontiers in aging neuroscience · 2022Article
- Article
- An In Vitro Model of the Blood-Brain Barrier to Study Alzheimer's Disease: The Role of β-Amyloid and Its Influence on PBMC Infiltration.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Reactive astrocytes: The nexus of pathological and clinical hallmarks of Alzheimer's disease.Ageing research reviews · 2021Review
- Article
- Small Vessel Disease-Related Dementia: An Invalid Neurovascular Coupling?International journal of molecular sciences · 2020Review
- The roles of dystroglycan in the nervous system: insights from animal models of muscular dystrophy.Disease models & mechanisms · 2018Review
- An emerging role of astrocytes in vascular contributions to cognitive impairment and dementia.Journal of neurochemistry · 2018Review
- Astrocyte Activation and the Calcineurin/NFAT Pathway in Cerebrovascular Disease.Frontiers in aging neuroscience · 2018Review
- Pathophysiology of Trans-Synaptic Adhesion Molecules: Implications for Epilepsy.Frontiers in cell and developmental biology · 2018Review
- Time-course of glial changes in the hyperhomocysteinemia model of vascular cognitive impairment and dementia (VCID).Neuroscience · 2017Article
- Recombinant Human Erythropoietin Protects Myocardial Cells from Apoptosis via the Janus-Activated Kinase 2/Signal Transducer and Activator of Transcription 5 Pathway in Rats with Epilepsy.Current therapeutic research, clinical and experimental · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epilepsy is characterized by the abnormal activation of neurons in the cerebral cortex, but the molecular and cellular mechanisms contributing to the development of recurrent seizures are largely unknown. Recently, the critical involvement of astrocytes in the pathophysiology of epilepsy has been proposed. However, the nature of plastic modulations of astrocytic proteins in the epileptic cortex remains poorly understood. In this study, we utilized the zero magnesium in vitro model of epilepsy and examined the potential molecular changes of cortical astrocytes, focusing specifically on endfeet, where specialized biochemical compartments exist. We find that the continuous epileptic activation of neurons for 1 h decreases the expression level of β-dystroglycan (βDG) in acute cortical brain slices prepared from mice. This change is completely abolished by the pharmacological blockade of NMDA-type glutamate receptors as well as by matrix metalloproteinase inhibitors. Consistent with the highly specialized localization of βDG at astrocytic endfeet, where it plays a pivotal role in anchoring endfeet-enriched proteins in astrocytes, the down-regulation of βDG is accompanied by a decrease in the expression of AQP4 but not laminin. Importantly, this down-regulation of βDG persists for at least 1 h, even after the apparent recovery of neuronal activation. Finally, we show that the down-regulation of βDG is associated with the dysfunction of the endfeet at the blood-brain interface as a diffusion barrier. These results suggest that the sustained down-regulation of βDG leads to dysfunctions of astrocytic endfeet in the epileptic cerebral cortex and may contribute to the pathogenesis of epilepsy.
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.