The Contribution of TRPV4 Channels to Astrocyte Volume Regulation and Brain Edema Formation
| Autor: | Helena Pivonkova, Andrea Gálisová, Thuraya Awadová, Jan Malinsky, Zuzana Hermanova, Daniel Zucha, Daniel Jirák, Lukas Valihrach, Miroslava Anderova, Denisa Kirdajova, Mikael Kubista |
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| Rok vydání: | 2018 |
| Předmět: |
Male
0301 basic medicine TRPV4 Genetically modified mouse Primary Cell Culture TRPV Cation Channels Brain Edema Brain Ischemia Green fluorescent protein Brain ischemia 03 medical and health sciences Transient receptor potential channel 0302 clinical medicine Edema medicine Animals Mice Knockout Glial fibrillary acidic protein biology Chemistry General Neuroscience Infarction Middle Cerebral Artery medicine.disease Cell biology Mice Inbred C57BL 030104 developmental biology medicine.anatomical_structure Astrocytes biology.protein Female medicine.symptom 030217 neurology & neurosurgery Astrocyte |
| Zdroj: | Neuroscience. 394:127-143 |
| ISSN: | 0306-4522 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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