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
Identifikátory výsledku
Kód výsledku v 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>
Nalezeny alternativní kódy
RIV/00216208:11130/19:10395822
Výsledek na webu
<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>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
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
Popis výsledku v původním jazyce
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.
Název v anglickém jazyce
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
Popis výsledku anglicky
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.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
30103 - Neurosciences (including psychophysiology)
Návaznosti výsledku
Projekt
<a href="/cs/project/GA15-02760S" target="_blank" >GA15-02760S: Úloha aquaporinových kanálů AQP4 v rozvoji cytotoxického edému vyvolaného mozkovou ischémií/reperfúzí</a><br>
Návaznosti
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2019
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
European Journal of Neuroscience
ISSN
0953-816X
e-ISSN
—
Svazek periodika
50
Číslo periodika v rámci svazku
1
Stát vydavatele periodika
GB - Spojené království Velké Británie a Severního Irska
Počet stran výsledku
15
Strana od-do
1685-1699
Kód UT WoS článku
000477045600001
EID výsledku v databázi Scopus
2-s2.0-85061290181