The Contribution of TRPV4 Channels to Astrocyte Volume Regulation and Brain Edema Formation

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11130%2F18%3A10383558" target="_blank" >RIV/00216208:11130/18:10383558 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/68378041:_____/18:00501980 RIV/86652036:_____/18:00501980 RIV/00216208:11110/18:10383558 RIV/00023001:_____/18:00077414

Výsledek na webu

<a href="https://doi.org/10.1016/j.neuroscience.2018.10.028" target="_blank" >https://doi.org/10.1016/j.neuroscience.2018.10.028</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.neuroscience.2018.10.028" target="_blank" >10.1016/j.neuroscience.2018.10.028</a>

Jazyk výsledku

angličtina

Název v původním jazyce

The Contribution of TRPV4 Channels to Astrocyte Volume Regulation and Brain Edema Formation

Popis výsledku v původním jazyce

Transient receptor potential vanilloid type 4 (TRPV4) channels are involved in astrocyte volume regulation; however, only limited data exist about its mechanism in astrocytes in situ. We performed middle cerebral artery occlusion in adult mice, where we found twice larger edema 1 day after the insult in trpv4(-/-) mice compared to the controls, which was quantified using magnetic resonance imaging. This result suggests disrupted volume regulation in the brain cells in trpv4(-/-) mice leading to increased edema formation. The aim of our study was to elucidate whether TRPV4 channel-based volume regulation occurs in astrocytes in situ and whether the disrupted volume regulation in trpv4(-/-) mice might lead to higher edema formation after brain ischemia. For our experiments, we used trpv4(-/-) mice crossed with transgenic mice expressing enhanced green fluorescent protein (EGFP) under the control of the glial fibrillary acidic protein promoter, which leads to astrocyte visualization by EGFP expression. For quantification of astrocyte volume changes, we used two-dimensional (2D) and three-dimensional (3D) morphometrical approaches and a quantification algorithm based on fluorescence intensity changes during volume alterations induced by hypotonicity or by oxygen-glucose deprivation. In contrast to in vitro experiments, we found little evidence of the contribution of TRPV4 channels to volume regulation in astrocytes in situ in adult mice. Moreover, we only found a rare expression of TRPV4 channels in adult mouse astrocytes. Our data suggest that TRPV4 channels are not involved in astrocyte volume regulation in situ; however, they play a protective role during the ischemia-induced brain edema formation. (C) 2018 IBRO. Published by Elsevier Ltd. All rights reserved.

Název v anglickém jazyce

The Contribution of TRPV4 Channels to Astrocyte Volume Regulation and Brain Edema Formation

Popis výsledku anglicky

Transient receptor potential vanilloid type 4 (TRPV4) channels are involved in astrocyte volume regulation; however, only limited data exist about its mechanism in astrocytes in situ. We performed middle cerebral artery occlusion in adult mice, where we found twice larger edema 1 day after the insult in trpv4(-/-) mice compared to the controls, which was quantified using magnetic resonance imaging. This result suggests disrupted volume regulation in the brain cells in trpv4(-/-) mice leading to increased edema formation. The aim of our study was to elucidate whether TRPV4 channel-based volume regulation occurs in astrocytes in situ and whether the disrupted volume regulation in trpv4(-/-) mice might lead to higher edema formation after brain ischemia. For our experiments, we used trpv4(-/-) mice crossed with transgenic mice expressing enhanced green fluorescent protein (EGFP) under the control of the glial fibrillary acidic protein promoter, which leads to astrocyte visualization by EGFP expression. For quantification of astrocyte volume changes, we used two-dimensional (2D) and three-dimensional (3D) morphometrical approaches and a quantification algorithm based on fluorescence intensity changes during volume alterations induced by hypotonicity or by oxygen-glucose deprivation. In contrast to in vitro experiments, we found little evidence of the contribution of TRPV4 channels to volume regulation in astrocytes in situ in adult mice. Moreover, we only found a rare expression of TRPV4 channels in adult mouse astrocytes. Our data suggest that TRPV4 channels are not involved in astrocyte volume regulation in situ; however, they play a protective role during the ischemia-induced brain edema formation. (C) 2018 IBRO. Published by Elsevier Ltd. All rights reserved.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30103 - Neurosciences (including psychophysiology)

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2018

Kód důvěrnosti údajů

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

Název periodika

Neuroscience

ISSN

0306-4522

e-ISSN

—

Svazek periodika

394

Číslo periodika v rámci svazku

December

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

17

Strana od-do

127-143

Kód UT WoS článku

000451069300011

EID výsledku v databázi Scopus

2-s2.0-85055916209