Abstract
ZDHHC16 promoted neurocyte ferroptosis by suppression of CREB in a cerebral apoplexy model
- Xinyu People’s Hospital, China
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.
Keywords
ZDHHC16, CREB, ferroptosis, cerebral apoplexy, ubiquitination
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