ArticleCells2020
Aquaporin-4 Expression during Toxic and Autoimmune Demyelination.
Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- Following the curvature: Sulcal versus gyral cortical localization of cerebral microbleeds in cerebral amyloid angiopathy.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Article
- Review
- The Fluidic Connectome in Brain Disease: Integrating Aquaporin-4 Polarity with Multisystem Pathways in Neurodegeneration.International journal of molecular sciences · 2025Review
- Sex-Specific Effects ofInternational journal of molecular sciences · 2025Article
- Glymphatic dysfunction in multiple sclerosis and its association with disease pathology and disability.Multiple sclerosis (Houndmills, Basingstoke, England) · 2024Article
- Short-chain fatty acids suppresses astrocyte activation by amplifying Trp-AhR-AQP4 signaling in experimental autoimmune encephalomyelitis mice.Cellular and molecular life sciences : CMLS · 2024Article
- Star power: harnessing the reactive astrocyte response to promote remyelination in multiple sclerosis.Neural regeneration research · 2024Review
- Emergence of the brain-border immune niches and their contribution to the development of neurodegenerative diseases.Frontiers in immunology · 2024Review
- Astrocytes: Lessons Learned from the Cuprizone Model.International journal of molecular sciences · 2023Review
- Article
- The glymphatic system: a new perspective on brain diseases.Frontiers in aging neuroscience · 2023Review
- Cuprizone feeding induces swollen astrocyte endfeet.Pflugers Archiv : European journal of physiology · 2022Article
- Research Evidence of the Role of the Glymphatic System and Its Potential Pharmacological Modulation in Neurodegenerative Diseases.Journal of clinical medicine · 2022Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The water channel protein aquaporin-4 (AQP4) is required for a normal rate of water exchange across the blood-brain interface. Following the discovery that AQP4 is a possible autoantigen in neuromyelitis optica, the function of AQP4 in health and disease has become a research focus. While several studies have addressed the expression and function of AQP4 during inflammatory demyelination, relatively little is known about its expression during non-autoimmune-mediated myelin damage. In this study, we used the toxin-induced demyelination model cuprizone as well as a combination of metabolic and autoimmune myelin injury (i.e., Cup/EAE) to investigate AQP4 pathology. We show that during toxin-induced demyelination, diffuse AQP4 expression increases, while polarized AQP4 expression at the astrocyte endfeet decreases. The diffuse increased expression of AQP4 was verified in chronic-active multiple sclerosis lesions. Around inflammatory brain lesions, AQP4 expression dramatically decreased, especially at sites where peripheral immune cells penetrate the brain parenchyma. Humoral immune responses appear not to be involved in this process since no anti-AQP4 antibodies were detected in the serum of the experimental mice. We provide strong evidence that the diffuse increase in anti-AQP4 staining intensity is due to a metabolic injury to the brain, whereas the focal, perivascular loss of anti-AQP4 immunoreactivity is mediated by peripheral immune cells.
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Registered trials
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