ZDHHC16 promoted neurocyte ferroptosis by suppression of CREB in a cerebral apoplexy model

Dongmei Xu; Hua Liu; Xiaoyu Deng; Jifan Fu

doi:10.5114/fn.2024.145878

eISSN: 1509-572x
ISSN: 1641-4640

Folia Neuropathologica

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4/2024
vol. 62

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abstract:

Original paper

ZDHHC16 promoted neurocyte ferroptosis by suppression of CREB in a cerebral apoplexy model

Dongmei Xu

¹

,

Hua Liu

¹

,

Xiaoyu Deng

¹

,

Jifan Fu

¹

Xinyu People’s Hospital, China

Folia Neuropathol 2024; 62 (4): 386-395

DOI: https://doi.org/10.5114/fn.2024.145878

Online publish date: 2024/12/31

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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

EVENTS

ZDHHC16 promoted neurocyte ferroptosis by suppression of CREB in a cerebral apoplexy model

Dongmei Xu 1 , Hua Liu 1 , Xiaoyu Deng 1 , Jifan Fu 1

ZDHHC16, CREB, ferroptosis, cerebral apoplexy, ubiquitination

Dongmei Xu

¹

,

Hua Liu

¹

,

Xiaoyu Deng

¹

,

Jifan Fu

¹