Folia neuropathologica · 2024
ZDHHC16 promoted neurocyte ferroptosis by suppression of CREB in a cerebral apoplexy model.
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Xu Dongmei, Liu Hua, Deng Xiaoyu, Fu Jifan
Аннотация
INTRODUCTION: The present study explored the effects and possible mechanisms of ZDHHC16 in a model of cerebral apoplexy (CA).
MATERIAL AND METHODS: Patients with CA were collected from our hospital. Mice were used to establish an middle cerebral artery occlusion (MCAO) model.
RESULTS: ZDHHC16 levels in patients with CA were up-regulated. ZDHHC16 up-regulation promoted inflammation and accelerated mitochondrial damage in the in vitro model. ZDHHC16 gene up-regulation promoted ferroptosis of neurocytes. The inhibition of ZDHHC16 prevented cerebral apoplexy in the mouse model. ZDHHC16 up-regulation suppressed CREB through interlinkage of CREB by promoting CREB ubiquitination. CREB agonists inhibited the effects of ZDHHC16 up-regulation in the in vitro model. CREB inhibitor inhibited the effects of ZDHHC16 down-regulation in the in vitro model.
CONCLUSIONS: We conclude that ZDHHC16 promoted ferroptosis and inflammation in a model of CA through the suppression of CREB. The findings might be of benefit in the treatment of CA or other nervous system diseases.
MATERIAL AND METHODS: Patients with CA were collected from our hospital. Mice were used to establish an middle cerebral artery occlusion (MCAO) model.
RESULTS: ZDHHC16 levels in patients with CA were up-regulated. ZDHHC16 up-regulation promoted inflammation and accelerated mitochondrial damage in the in vitro model. ZDHHC16 gene up-regulation promoted ferroptosis of neurocytes. The inhibition of ZDHHC16 prevented cerebral apoplexy in the mouse model. ZDHHC16 up-regulation suppressed CREB through interlinkage of CREB by promoting CREB ubiquitination. CREB agonists inhibited the effects of ZDHHC16 up-regulation in the in vitro model. CREB inhibitor inhibited the effects of ZDHHC16 down-regulation in the in vitro model.
CONCLUSIONS: We conclude that ZDHHC16 promoted ferroptosis and inflammation in a model of CA through the suppression of CREB. The findings might be of benefit in the treatment of CA or other nervous system diseases.