The Contribution of TRPV4 Channels to Astrocyte Volume Regulation and Brain Edema Formation
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
30367945
DOI
10.1016/j.neuroscience.2018.10.028
PII: S0306-4522(18)30691-2
Knihovny.cz E-resources
- Keywords
- TRPV4 channels, astrocytes, ischemia, volume regulation,
- MeSH
- Astrocytes metabolism pathology MeSH
- Brain Edema etiology metabolism pathology MeSH
- Infarction, Middle Cerebral Artery metabolism pathology MeSH
- Brain Ischemia complications MeSH
- TRPV Cation Channels genetics metabolism MeSH
- Mice, Inbred C57BL MeSH
- Mice, Knockout MeSH
- Primary Cell Culture MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- TRPV Cation Channels MeSH
- Trpv4 protein, mouse MeSH Browser
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.
References provided by Crossref.org
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Astrocytic TRPV4 Channels and Their Role in Brain Ischemia
