• Je něco špatně v tomto záznamu ?

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

H. Pivonkova, Z. Hermanova, D. Kirdajova, T. Awadova, J. Malinsky, L. Valihrach, D. Zucha, M. Kubista, A. Galisova, D. Jirak, M. Anderova,

. 2018 ; 394 (-) : 127-143. [pub] 20181024

Jazyk angličtina Země Spojené státy americké

Typ dokumentu časopisecké články, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/bmc19012215

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.

Citace poskytuje Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc19012215
003      
CZ-PrNML
005      
20190418082359.0
007      
ta
008      
190405s2018 xxu f 000 0|eng||
009      
AR
024    7_
$a 10.1016/j.neuroscience.2018.10.028 $2 doi
035    __
$a (PubMed)30367945
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a xxu
100    1_
$a Pivonkova, Helena $u Department of Cellular Neurophysiology, Institute of Experimental Medicine, Czech Academy of Sciences, Prague, Czech Republic.
245    14
$a The Contribution of TRPV4 Channels to Astrocyte Volume Regulation and Brain Edema Formation / $c H. Pivonkova, Z. Hermanova, D. Kirdajova, T. Awadova, J. Malinsky, L. Valihrach, D. Zucha, M. Kubista, A. Galisova, D. Jirak, M. Anderova,
520    9_
$a 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.
650    _2
$a zvířata $7 D000818
650    _2
$a astrocyty $x metabolismus $x patologie $7 D001253
650    _2
$a edém mozku $x etiologie $x metabolismus $x patologie $7 D001929
650    _2
$a ischemie mozku $x komplikace $7 D002545
650    _2
$a ženské pohlaví $7 D005260
650    _2
$a infarkt arteria cerebri media $x metabolismus $x patologie $7 D020244
650    _2
$a mužské pohlaví $7 D008297
650    _2
$a myši inbrední C57BL $7 D008810
650    _2
$a myši knockoutované $7 D018345
650    _2
$a primární buněčná kultura $7 D061251
650    _2
$a kationtové kanály TRPV $x genetika $x metabolismus $7 D050916
655    _2
$a časopisecké články $7 D016428
655    _2
$a práce podpořená grantem $7 D013485
700    1_
$a Hermanova, Zuzana $u Department of Cellular Neurophysiology, Institute of Experimental Medicine, Czech Academy of Sciences, Prague, Czech Republic.
700    1_
$a Kirdajova, Denisa $u Department of Cellular Neurophysiology, Institute of Experimental Medicine, Czech Academy of Sciences, Prague, Czech Republic.
700    1_
$a Awadova, Thuraya $u Department of Microscopy, Institute of Experimental Medicine, Czech Academy of Sciences, Prague, Czech Republic.
700    1_
$a Malinsky, Jan $u Department of Microscopy, Institute of Experimental Medicine, Czech Academy of Sciences, Prague, Czech Republic.
700    1_
$a Valihrach, Lukas $u Laboratory of Gene Expression, Institute of Biotechnology, Czech Academy of Sciences, Prague, Czech Republic.
700    1_
$a Zucha, Daniel $u Laboratory of Gene Expression, Institute of Biotechnology, Czech Academy of Sciences, Prague, Czech Republic.
700    1_
$a Kubista, Mikael $u Laboratory of Gene Expression, Institute of Biotechnology, Czech Academy of Sciences, Prague, Czech Republic; TATAA Biocenter AB, Gothenburg 411 03, Sweden.
700    1_
$a Galisova, Andrea $u Department of Radiodiagnostic and Interventional Radiology, Institute of Clinical and Experimental Medicine, Prague, Czech Republic.
700    1_
$a Jirak, Daniel $u Department of Radiodiagnostic and Interventional Radiology, Institute of Clinical and Experimental Medicine, Prague, Czech Republic; Institute of Biophysics and Informatics, 1st Medicine Faculty, Charles University, Prague, Czech Republic.
700    1_
$a Anderova, Miroslava $u Department of Cellular Neurophysiology, Institute of Experimental Medicine, Czech Academy of Sciences, Prague, Czech Republic; Department of Neuroscience, 2nd Medical Faculty, Charles University, Prague, Czech Republic. Electronic address: anderova@biomed.cas.cz.
773    0_
$w MED00003505 $t Neuroscience $x 1873-7544 $g Roč. 394, č. - (2018), s. 127-143
856    41
$u https://pubmed.ncbi.nlm.nih.gov/30367945 $y Pubmed
910    __
$a ABA008 $b sig $c sign $y a $z 0
990    __
$a 20190405 $b ABA008
991    __
$a 20190418082427 $b ABA008
999    __
$a ok $b bmc $g 1391525 $s 1050520
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2018 $b 394 $c - $d 127-143 $e 20181024 $i 1873-7544 $m Neuroscience $n Neuroscience $x MED00003505
LZP    __
$a Pubmed-20190405

Najít záznam

Citační ukazatele

Možnosti archivace