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

Result code in 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>

Alternative codes found

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

Result on the web

<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>

Result language

angličtina

Original language name

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

Original language description

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.

Czech name

—

Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

—

OECD FORD branch

30103 - Neurosciences (including psychophysiology)

Project

Result was created during the realization of more than one project. More information in the Projects tab.

Continuities

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

Publication year

2018

Confidentiality

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

Name of the periodical

Neuroscience

ISSN

0306-4522

e-ISSN

—

Volume of the periodical

394

Issue of the periodical within the volume

December

Country of publishing house

US - UNITED STATES

Number of pages

17

Pages from-to

127-143

UT code for WoS article

000451069300011

EID of the result in the Scopus database

2-s2.0-85055916209