| First Author | Mak KM | Year | 2012 |
| Journal | Neurosignals | Volume | 20 |
| Issue | 4 | Pages | 237-51 |
| PubMed ID | 23172129 | Mgi Jnum | J:317821 |
| Mgi Id | MGI:6855176 | Doi | 10.1159/000331899 |
| Citation | Mak KM, et al. (2012) Nuclear factor of activated T cells 5 deficiency increases the severity of neuronal cell death in ischemic injury. Neurosignals 20(4):237-51 |
| abstractText | 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. |
