ArticleThe European journal of neuroscience2017
Hypothermia increases aquaporin 4 (AQP4) plasma membrane abundance in human primary cortical astrocytes via a calcium/transient receptor potential vanilloid 4 (TRPV4)- and calmodulin-mediated mechanism.
Article in The European journal of neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.
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Who cites it
69 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.
- Mechanisms Underlying Aquaporin-4 Subcellular Mislocalization in Epilepsy.Frontiers in cellular neuroscience · 2022Pooled it
- Spatial organization of AQP4 water channel expression in the human brain.Science advances · 2026Article
- Written in the Stars: Astrocyte Biology From Evolution to Disease.Acta physiologica (Oxford, England) · 2026Review
- The Dual Role of Macroglia in Glaucoma: Deciphering the Contributions of Astrocytes and Müller Cells to Retinal Neurodegeneration and Neuroprotection.International journal of molecular sciences · 2026Review
- Repeated moderate hypothermia leads to sustained glymphatic dysfunction and loss of vascular AQP4 polarization.Fluids and barriers of the CNS · 2026Article
- Distinct AQP4 Alterations in Movement Disorders with Primary Synucleinopathy.Movement disorders : official journal of the Movement Disorder Society · 2025Article
- Potentiating Cerebral Perfusion Normalizes Glymphatic Dynamics in Systemic Inflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Bridging the barrier: insights into blood biomarkers and therapeutic strategies targeting choroid plexus and BBB dysfunction in alzheimer's disease.Biomarker research · 2025Review
- The Cerebral Lymphatic System: Function, Controversies, and Therapeutic Approaches for Central Nervous System Diseases.Cellular and molecular neurobiology · 2025Review
- Osteopontin Regulates AQP4 Expression by TRPV4 Activation in Müller Cells: Implications for Retinal Homeostasis.Molecular neurobiology · 2025Article
- Very Low-Intensity Ultrasound Facilitates Glymphatic Influx and Clearance via Modulation of the TRPV4-AQP4 Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
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- Non-coding RNAs and Aquaporin 4: Their Role in the Pathogenesis of Neurological Disorders.Neurochemical research · 2024Review
- Mechanisms of aquaporin-4 vesicular trafficking in mammalian cells.Journal of neurochemistry · 2024Article
- The Role of Astrocytes in Parkinson's Disease : Astrocytes in Parkinson's Disease.Advances in neurobiology · 2024Review
- The deletion of AQP4 and TRPV4 affects astrocyte swelling/volume recovery in response to ischemia-mimicking pathologies.Frontiers in cellular neuroscience · 2024Article
- Angelicin Alleviates Maternal Isoflurane Exposure-Induced Offspring Cognitive Defects Through the Carbonic Anhydrase 4/Aquaporin-4 Pathway.Molecular biotechnology · 2024Article
- Cation flux through SUR1-TRPM4 and NCX1 in astrocyte endfeet induces water influx through AQP4 and brain swelling after ischemic stroke.Science signaling · 2023Article
- Pathophysiology and Neuroimmune Interactions Underlying Parkinson's Disease and Traumatic Brain Injury.International journal of molecular sciences · 2023Review
9 more citing papers are in PubMed but not listed here.
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 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human aquaporin 4 (AQP4) is the primary water channel protein in brain astrocytes. Hypothermia is known to cause astrocyte swelling in culture, but the precise role of AQP4 in this process is unknown. Primary human cortical astrocytes were cultured under hypothermic (32 °C) or normothermic (37 °C) conditions. AQP4 transcript, total protein and surface-localized protein were quantified using RT-qPCR, sandwich ELISA with whole cell lysates or cell surface biotinylation, followed by ELISA analysis of the surface-localized protein, respectively. Four-hour mild hypothermic treatment increased the surface localization of AQP4 in human astrocytes to 155 ± 4% of normothermic controls, despite no change in total protein expression levels. The hypothermia-mediated increase in AQP4 surface abundance on human astrocytes was blocked using either calmodulin antagonist (trifluoperazine, TFP); TRPV4 antagonist, HC-067047 or calcium chelation using EGTA-AM. The TRPV4 agonist (GSK1016790A) mimicked the effect of hypothermia compared with untreated normothermic astrocytes. Hypothermia led to an increase in surface localization of AQP4 in human astrocytes through a mechanism likely dependent on the TRPV4 calcium channel and calmodulin activation. Understanding the effects of hypothermia on astrocytic AQP4 cell surface expression may help develop new treatments for brain swelling based on an in-depth mechanistic understanding of AQP4 translocation.
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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.