Na+, K+-ATPase dysfunction causes cerebrovascular endothelial cell degeneration in rat prefrontal cortex slice cultures
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- 作者：Yuki Kurauchia ; Akinori Hisatsuneb ; c ; Takahiro Sekia ; Hiroshi Katsukia ; hkatsuki@gpo.kumamoto-u.ac.jp" class="auth_mail" title="E-mail the corresponding author
- 关键词：CBF ; cerebral blood flow ; DMSO ; dimethylsulfoxide ; ER ; endoplasmic reticulum ; GSK3β ; glycogen synthase kinase 3β ; IP3 receptor ; inositol triphosphate receptor ; MAPK ; mitogen-activated protein kinase ; mTOR ; mammalian target of rapamycin ; NCX ; Na+ ; Ca2+ exchanger ; PI3-kinase ; phosphoinositide 3-kinase ; PDGFRβ ; platelet-derived growth factor receptor β ; PFC ; prefrontal cortex ; RECA-1 ; rat endothelial cell antigen-1 ; SDS ; sodium dodecyl sulfate
- 刊名：Brain Research
- 出版年：2016
- 出版时间：1 August 2016
- 年：2016
- 卷：1644
- 期：Complete
- 页码：249-257
- 全文大小：1883 K
文摘
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We evaluated cerebrovascular unit structure in novel organotypic slice culture model.
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Na+, K+-ATPase inhibition causes cerebrovascular endothelial cell degeneration.
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IP3 receptor-mediated Ca2+ release is involved in endothelial cell degeneration.
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Inactivation of GSK3β protects cerebrovascular endothelial cells.