Aquaporin-4 Expression
Aquaporin-4 Expression - Related Videos
04:21
An Assay to Detect Serum Anti-aquaporin-4 Immunoglobulin G
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2025
The video demonstrates a cell-based assay for detecting anti-aquaporin-4 immunoglobulin G using a biochip containing untransfected cells and transfected cells expressing aquaporin-4. This method has applications in diagnosing neuromyelitis optica spectrum disorders, confirmed by strong green fluorescence on the biochip.
01:56
Inducing Paralysis in a Mouse Model via Transfer of Aquaporin-4-Specific Th17 Cells
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2025
This video demonstrates the procedure of inducing paralysis by transferring activated Th17 cells targeting aquaporin-4 into a mouse model. In the central nervous system, the activated Th17 cells interact with aquaporin-4-expressing astrocytes, triggering an immune response that leads to tail and limb paralysis in the mouse.
09:29
Induction of Paralysis and Visual System Injury in Mice by T Cells Specific for Neuromyelitis Optica Autoantigen Aquaporin-4
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Cited by 10 •
2017
Here, we present a protocol to induce paralysis and opticospinal inflammation by transfer of aquaporin-4 (AQP4)-specific T cells from AQP4-/- mice into WT mice. In addition, we demonstrate how to use serial optical coherence tomography to monitor visual system dysfunction.
05:45
Human Serum Anti-aquaporin-4 Immunoglobulin G Detection by Cell-based Assay
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Cited by 5 •
2019
Cell-based assay is a widely used method to detect serum anti-aquaporin-4 immunoglobulin G. This method could be applied to clinical diagnosis and scientific researches of neuromyelitis optical spectrum disorders.
01:25
Aquaporins
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2023
Aquaporins or AQPs are a family of integral membrane proteins whose primary function is to transport water, while some called aquaglyceroporins also transport glycerol. In addition, aquaporins have also been suspected to be involved in transporting volatile substances, such as carbon dioxide and ammonia, across membranes. Such AQPs that act as gas channels are often highly expressed in cells involved in the gaseous exchange, such as red blood cells, epithelial cells, and pulmonary capillaries.
FAQs
AQP4 expression depends on a sequence of linked cellular events. Gene transcription generates AQP4 mRNA, which is translated into the channel protein, while membrane-trafficking and anchoring mechanisms position that protein at astrocyte endfeet. Examining these stages separately helps researchers determine whether altered AQP4 reflects changes in production, delivery to the membrane, or retention at the blood–brain barrier.
Location is as important as protein production. Concentrating AQP4 in astrocyte endfeet places the water channel at a key interface associated with the blood–brain barrier, allowing its distribution to contribute to central nervous system fluid regulation. A change in placement could therefore alter water handling even when total AQP4 production does not change in the same way.
AQP4-directed autoantibodies provide an immunological context for studying neuromyelitis optica. Their association with astrocyte damage links an immune response against AQP4 with disrupted water transport, edema, and neurological disease. Measuring expression and localization alongside antibody-related effects can help connect molecular changes in astrocytes with tissue-level consequences in the central nervous system.
A useful assessment considers both how much AQP4 is produced and where it is positioned. AQP4 mRNA reflects transcriptional output, while the protein and its distribution at astrocyte endfeet provide information about translation and membrane placement. Comparing these features with normal tissue can help distinguish altered fluid regulation from changes associated with inflammation, infection, or injury.
Interpretation requires comparison with the expected astrocyte pattern rather than relying on a single expression value. Differences in AQP4 production or endfoot placement may indicate disrupted water regulation, but their significance depends on the surrounding context of neuroinflammation, infection, or tissue injury. This approach helps relate molecular observations to edema and astrocyte damage without treating every change as equivalent.
In immunology and infection research, AQP4 expression connects astrocyte biology with inflammatory and tissue responses in the central nervous system. Expression measurements can reveal whether water-regulatory features change during neuroinflammation, infection, or injury, while AQP4-directed autoantibodies provide a disease-specific immune context through neuromyelitis optica. Together, these observations support analysis of edema, astrocyte damage, and neurological outcomes.