Neuro-signals | |
Nuclear Factor of Activated T Cells 5 Deficiency Increases the Severity of Neuronal Cell Death in Ischemic Injury | |
关键词: Knockout; NFAT5; Ischemia; SMIT; Oxidative stress; | |
DOI : 10.1159/000331899 | |
学科分类:神经科学 | |
来源: S Karger AG | |
【 摘 要 】
Nuclear factor of activated T cells 5 (NFAT5) has been implicated in regulating several genes that are thought to be neuroprotective in ischemic injury. Because of the embryonic lethality of NFAT5 knockout (NFAT5–/–) mice, the heterozygous (NFAT5+/–) mice were used to study the in vivo role of NFAT5 in hypoxia/ischemia (H/I) condition. The NFAT5+/– mice exhibited more severe neurological deficits, larger infarct area and edema formation associated with increased aquaporin 4 expressions in the brain. Under in vitro H/I condition, increased apoptotic cell death was found in NFAT5–/– neurons. Moreover, SMIT, a downstream to NFAT5, was upregulated in NFAT5+/+ neurons, while the SMIT level could not be upregulated in NFAT5–/– neurons under H/I condition. The elevation of reactive oxygen species generation in NFAT5–/– neurons under H/I condition further confirmed that NFAT5–/– neurons were more susceptible to oxidative stress. The present study demonstrated that activation of NFAT5 and its downstream SMIT induction is important in protecting neurons from ischemia-induced oxidative stress.
【 授权许可】
CC BY-NC-ND
【 预 览 】
Files | Size | Format | View |
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RO201904039698392ZK.pdf | 1486KB | download |