ArticlePloS one2016
Aquaporin-4 Cell-Surface Expression and Turnover Are Regulated by Dystroglycan, Dynamin, and the Extracellular Matrix in Astrocytes.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- The Role of Aquaporins in Epileptogenesis-A Systematic Review.International journal of molecular sciences · 2023Pooled it
- Sleep-circadian modulation of autophagy and glymphatic function: failure of coordinated brain clearance in Parkinson's disease.NPJ Parkinson's disease · 2026Review
- Site-Specific Phosphoproteomic Profiling of CAV1 Reveals Co-Regulatory Kinase Networks in Cancer Signaling.International journal of molecular sciences · 2026Article
- The postnatal expression of transcripts and proteins in the corpus callosum, as well as its myelinization, is affected by the congenital absence of AQP4.Journal of physiology and biochemistry · 2026Article
- Mild traumatic brain injury promotes chronic cerebrovascular inflammation and glymphatic suppression.Molecular neurodegeneration advances · 2026Article
- Potentiating Cerebral Perfusion Normalizes Glymphatic Dynamics in Systemic Inflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Targeting TRPV4 to restore glymphatic system function and alleviate cerebral edema in ischemic stroke.Brain pathology (Zurich, Switzerland) · 2025Article
- Article
- Membrane trafficking of synaptic adhesion molecules.The Journal of physiology · 2025Review
- Osteopontin Regulates AQP4 Expression by TRPV4 Activation in Müller Cells: Implications for Retinal Homeostasis.Molecular neurobiology · 2025Article
- Remote Regulation of Molecular Diffusion in Extracellular Space of Parkinson's Disease Rat Model by Subthalamic Nucleus Deep Brain Stimulation.Cyborg and bionic systems (Washington, D.C.) · 2025Article
- AQP4 Endocytosis-Lysosome Degradation Mediated by MMP-9/β-DG Involved in Diabetes Cognitive Impairment.Molecular neurobiology · 2024Article
- Impact of aquaporin-4 and CD11c + microglia in the development of ependymal cells in the aqueduct: inferences to hydrocephalus.Fluids and barriers of the CNS · 2024Article
- Mechanisms of aquaporin-4 vesicular trafficking in mammalian cells.Journal of neurochemistry · 2024Article
- Aquaporin-4 Expression Switches from White to Gray Matter Regions during Postnatal Development of the Central Nervous System.International journal of molecular sciences · 2023Article
- Molecular mechanisms governing aquaporin relocalisation.Biochimica et biophysica acta. Biomembranes · 2022Review
- Cellular Distribution of Brain Aquaporins and Their Contribution to Cerebrospinal Fluid Homeostasis and Hydrocephalus.Biomolecules · 2022Review
- The cell adhesion protein dystroglycan affects the structural remodeling of dendritic spines.Scientific reports · 2022Article
- Astrocyte depletion alters extracellular matrix composition in the demyelinating phase of Theiler's murine encephalomyelitis.PloS one · 2022Article
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The water-permeable channel aquaporin-4 (AQP4) is highly expressed in perivascular astrocytes of the mammalian brain and represents the major conduit for water across the blood-brain barrier. Within these cells, AQP4 is found in great quantities at perivascular endfoot sites but is detected in lesser amounts at the membrane domains within the brain parenchyma. We had previously established that this polarization was regulated by the interaction between dystroglycan (DG), an extracellular matrix receptor that is co-expressed with AQP4, and the laminin that is contained within the perivascular basal lamina. In the present study, we have attempted to describe the mechanisms that underlie this regulation, using primary astrocyte cultures. Via biotinylation, we found that the cell-surface expression of AQP4 is DG-dependent and is potentiated by laminin. We also determined that this laminin-dependent increase occurs not through an upregulation of total AQP4 levels, but rather from a redirection of AQP4 from an intracellular, EEA-1-associated pool to the cell surface. We then demonstrated an association between DG and dynamin and showed that dynamin functioned in conjunction with clathrin to regulate surface AQP4 amounts. Furthermore, we observed that DG preferentially binds to the inactive forms of dynamin, suggesting that this interaction was inhibitory for AQP4 endocytosis. Finally, we showed that laminin selectively upregulates the cell-surface expression of the M23 isoform of AQP4. Our data therefore indicate that the dual interation of DG with laminin and dynamin is involved in the regulation of AQP4 internalization, leading to its asymmetric enrichment at perivascular astrocyte endfeet.
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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.