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The role of aquaporin-4 and transient receptor potential vaniloid isoform 4 channels in the development of cytotoxic edema and associated extracellular diffusion parameter changes

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378041%3A_____%2F19%3A00508398" target="_blank" >RIV/68378041:_____/19:00508398 - isvavai.cz</a>

  • Alternative codes found

    RIV/00216208:11130/19:10395822

  • Result on the web

    <a href="https://onlinelibrary.wiley.com/doi/abs/10.1111/ejn.14338" target="_blank" >https://onlinelibrary.wiley.com/doi/abs/10.1111/ejn.14338</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1111/ejn.14338" target="_blank" >10.1111/ejn.14338</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    The role of aquaporin-4 and transient receptor potential vaniloid isoform 4 channels in the development of cytotoxic edema and associated extracellular diffusion parameter changes

  • Original language description

    The proper function of the nervous system is dependent on the balance of ions and water between the intracellular and extracellular space (ECS). It has been suggested that the interaction of aquaporin-4 (AQP4) and the transient receptor potential vaniloid isoform 4 (TRPV4) channels play a role in water balance and cell volume regulation, and indirectly, of the ECS volume. Using the real-time iontophoretic method, we studied the changes of the ECS diffusion parameters: ECS volume fraction alpha (alpha = ECS volume fraction/total tissue volume) and tortuosity lambda (lambda(2) = free/apparent diffusion coefficient) in mice with a genetic deficiency of AQP4 or TRPV4 channels, and in control animals. The used models of cytotoxic edema included: mild and severe hypotonic stress or oxygen-glucose deprivation (OGD) in situ and terminal ischemia/anoxia in vivo. This study shows that an AQP4 or TRPV4 deficit slows down the ECS volume shrinkage during severe ischemia in vivo. We further demonstrate that a TRPV4 deficit slows down the velocity and attenuates an extent of the ECS volume decrease during OGD treatment in situ. However, in any of the cytotoxic edema models in situ (OGD, mild or severe hypotonic stress), we did not detect any alterations in the cell swelling or volume regulation caused by AQP4 deficiency. Overall, our results indicate that the AQP4 and TRPV4 channels may play a crucial role in severe pathological states associated with their overexpression and enhanced cell swelling. However, detailed interplay between AQP4 and TRPV4 channels requires further studies and additional research.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30103 - Neurosciences (including psychophysiology)

Result continuities

  • Project

    <a href="/en/project/GA15-02760S" target="_blank" >GA15-02760S: Role of the aquaporin channel AQP4 in the development of cytotoxic brain edema following brain ischemia/reperfusion</a><br>

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2019

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    European Journal of Neuroscience

  • ISSN

    0953-816X

  • e-ISSN

  • Volume of the periodical

    50

  • Issue of the periodical within the volume

    1

  • Country of publishing house

    GB - UNITED KINGDOM

  • Number of pages

    15

  • Pages from-to

    1685-1699

  • UT code for WoS article

    000477045600001

  • EID of the result in the Scopus database

    2-s2.0-85061290181