ArticleThe Journal of biological chemistry2009
Interdependence of laminin-mediated clustering of lipid rafts and the dystrophin complex in astrocytes.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
- Astrocyte Enrichment of 3D Cortical Constructs Enhances Brain Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 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
- The Laminin-Induced Phosphorylation of PKCδ Regulates AQP4 Distribution and Water Permeability in Rat Astrocytes.Cellular and molecular neurobiology · 2021Article
- Article
- Review
- Organisation of extracellular matrix proteins laminin and agrin in pericapillary basal laminae in mouse brain.Brain structure & function · 2020Article
- Appearance of β-dystroglycan precedes the formation of glio-vascular end-feet in developing rat brain.European journal of histochemistry : EJH · 2018Article
- Determining Cell-surface Expression and Endocytic Rate of Proteins in Primary Astrocyte Cultures Using Biotinylation.Journal of visualized experiments : JoVE · 2017Article
- The Oxidative Stress-Induced Increase in the Membrane Expression of the Water-Permeable Channel Aquaporin-4 in Astrocytes Is Regulated by Caveolin-1 Phosphorylation.Frontiers in cellular neuroscience · 2017Article
- Aquaporin-4 Cell-Surface Expression and Turnover Are Regulated by Dystroglycan, Dynamin, and the Extracellular Matrix in Astrocytes.PloS one · 2016Article
- The central role of aquaporins in the pathophysiology of ischemic stroke.Frontiers in cellular neuroscience · 2015Review
- Lost Polarization of Aquaporin4 and Dystroglycan in the Core Lesion after Traumatic Brain Injury Suggests Functional Divergence in Evolution.BioMed research international · 2015Article
- The extracellular matrix protein laminin α2 regulates the maturation and function of the blood-brain barrier.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Sustained down-regulation of β-dystroglycan and associated dysfunctions of astrocytic endfeet in epileptic cerebral cortex.The Journal of biological chemistry · 2014Article
- Physiological roles of aquaporin-4 in brain.Physiological reviews · 2013Review
- Ordered disorder of the astrocytic dystrophin-associated protein complex in the norm and pathology.PloS one · 2013Article
- Water permeability of aquaporin-4 channel depends on bilayer composition, thickness, and elasticity.Biophysical journal · 2012Article
- Expression of dystrophins and the dystrophin-associated-protein complex by pituicytes in culture.Neurochemical research · 2011Article
- Regulation of Kir4.1 and AQP4 expression and stability at the basolateral domain of epithelial MDCK cells by the extracellular matrix.American journal of physiology. Renal physiology · 2011Article
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
Astrocyte endfeet surrounding blood vessels are active domains involved in water and potassium ion transport crucial to the maintenance of water and potassium ion homeostasis in brain. A growing body of evidence points to a role for dystroglycan and its interaction with perivascular laminin in the targeting of the dystrophin complex and the water-permeable channel, aquaporin 4 (AQP4), at astrocyte endfeet. However, the mechanisms underlying such compartmentalization remain poorly understood. In the present study we found that AQP4 resided in Triton X-100-insoluble fraction, whereas dystroglycan was recovered in the soluble fraction in astrocytes. Cholesterol depletion resulted in the translocation of a pool of AQP4 to the soluble fraction indicating that its distribution is indeed associated with cholesterol-rich membrane domains. Upon laminin treatment AQP4 and the dystrophin complex, including dystroglycan, reorganized into laminin-associated clusters enriched for the lipid raft markers GM1 and flotillin-1 but not caveolin-1. Reduced diffusion rates of GM1 in the laminin-induced clusters were indicative of the reorganization of raft components in these domains. In addition, both cholesterol depletion and dystroglycan silencing reduced the number and area of laminin-induced clusters of GM1, AQP4, and dystroglycan. These findings demonstrate the interdependence between laminin binding to dystroglycan and GM1-containing lipid raft reorganization and provide novel insight into the dystrophin complex regulation of AQP4 polarization in astrocytes.
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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.