ArticleGlia2012
Molecular scaffolds underpinning macroglial polarization: an analysis of retinal Müller cells and brain astrocytes in mouse.
Article in Glia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
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Who cites it
21 citing papers in PubMed.
- The missense mutation C667F in murine β-dystroglycan causes embryonic lethality, myopathy and blood-brain barrier destabilization.Disease models & mechanisms · 2024Article
- Neonatal stress disrupts the glymphatic system development and increases the susceptibility to Parkinson's disease in later life.CNS neuroscience & therapeutics · 2024Article
- Glia as a key factor in cell volume regulation processes of the central nervous system.Frontiers in cellular neuroscience · 2022Review
- The pathogenesis of idiopathic normal pressure hydrocephalus based on the understanding of AQP1 and AQP4.Frontiers in molecular neuroscience · 2022Review
- Uncoupling the Excitatory Amino Acid Transporter 2 From Its C-Terminal Interactome Restores Synaptic Glutamate Clearance at Corticostriatal Synapses and Alleviates Mutant Huntingtin-Induced Hypokinesia.Frontiers in cellular neuroscience · 2021Article
- Astrocytic CaFrontiers in cellular neuroscience · 2021Review
- Functional specialization of retinal Müller cell endfeet depends on an interplay between two syntrophin isoforms.Molecular brain · 2020Article
- The Regional Specific Alterations in BBB Permeability are Relevant to the Differential Responses of 67-kDa LR Expression in Endothelial Cells and Astrocytes Following Status Epilepticus.International journal of molecular sciences · 2019Article
- Chronic stress impairs the aquaporin-4-mediated glymphatic transport through glucocorticoid signaling.Psychopharmacology · 2019Article
- Dysfunction of 67-kDa Laminin Receptor Disrupts BBB Integrity via Impaired Dystrophin/AQP4 Complex and p38 MAPK/VEGF Activation Following Status Epilepticus.Frontiers in cellular neuroscience · 2019Article
- A transcriptome-based assessment of the astrocytic dystrophin-associated complex in the developing human brain.Journal of neuroscience research · 2018Article
- Human and mouse cortical astrocytes differ in aquaporin-4 polarization toward microvessels.Glia · 2017Article
- Aquaporin-4 in Astroglial Cells in the CNS and Supporting Cells of Sensory Organs-A Comparative Perspective.International journal of molecular sciences · 2016Review
- Aquaporin-4 and Cerebrovascular Diseases.International journal of molecular sciences · 2016Review
- Characterization of a Dmd (EGFP) reporter mouse as a tool to investigate dystrophin expression.Skeletal muscle · 2016Article
- Augmentation of Ca(2+) signaling in astrocytic endfeet in the latent phase of temporal lobe epilepsy.Frontiers in cellular neuroscience · 2015Article
- Evidence that pericytes regulate aquaporin-4 polarization in mouse cortical astrocytes.Brain structure & function · 2014Article
- Hepatocyte growth factor promotes long-term survival and axonal regeneration of retinal ganglion cells after optic nerve injury: comparison with CNTF and BDNF.CNS neuroscience & therapeutics · 2014Article
- Aggregation state determines the localization and function of M1- and M23-aquaporin-4 in astrocytes.The Journal of cell biology · 2014Article
- Physiological roles of aquaporin-4 in brain.Physiological reviews · 2013Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Key roles of macroglia are inextricably coupled to specialized membrane domains. The perivascular endfoot membrane has drawn particular attention, as this domain contains a unique complement of aquaporin-4 (AQP4) and other channel proteins that distinguishes it from perisynaptic membranes. Recent studies indicate that the polarization of macroglia is lost in a number of diseases, including temporal lobe epilepsy and Alzheimer's disease. A better understanding is required of the molecular underpinning of astroglial polarization, particularly when it comes to the significance of the dystrophin associated protein complex (DAPC). Here, we employ immunofluorescence and immunogold cytochemistry to analyze the molecular scaffolding in perivascular endfeet in macroglia of retina and three regions of brain (cortex, dentate gyrus, and cerebellum), using AQP4 as a marker. Compared with brain astrocytes, Müller cells (a class of retinal macroglia) exhibit lower densities of the scaffold proteins dystrophin and α-syntrophin (a DAPC protein), but higher levels of AQP4. In agreement, depletion of dystrophin or α-syntrophin--while causing a dramatic loss of AQP4 from endfoot membranes of brain astrocytes--had only modest or insignificant effect, respectively, on the AQP4 pool in endfoot membranes of Müller cells. In addition, while polarization of brain macroglia was less affected by dystrophin depletion than by targeted deletion of α-syntrophin, the reverse was true for retinal macroglia. These data indicate that the molecular scaffolding in perivascular endfeet is more complex than previously assumed and that macroglia are heterogeneous with respect to the mechanisms that dictate their polarization.
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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.