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

IF 1.5 4区医学 Q4 NEUROSCIENCES

Folia neuropathologica Pub Date : 2024-01-01 DOI:10.5114/fn.2024.145878

Dongmei Xu, Hua Liu, Xiaoyu Deng, Jifan Fu

{"title":"ZDHHC16 promoted neurocyte ferroptosis by suppression of CREB in a cerebral apoplexy model.","authors":"Dongmei Xu, Hua Liu, Xiaoyu Deng, Jifan Fu","doi":"10.5114/fn.2024.145878","DOIUrl":null,"url":null,"abstract":"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.","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":"62 4","pages":"386-395"},"PeriodicalIF":1.5000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Folia neuropathologica","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.5114/fn.2024.145878","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"NEUROSCIENCES","Score":null,"Total":0}

引用次数: 0

Abstract

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.

查看原文本刊更多论文

求助全文

约1分钟内获得全文求助全文

来源期刊

Folia neuropathologica 医学-病理学

CiteScore

2.50

自引率

5.00%

发文量

审稿时长

>12 weeks

期刊介绍： Folia Neuropathologica is an official journal of the Mossakowski Medical Research Centre Polish Academy of Sciences and the Polish Association of Neuropathologists. The journal publishes original articles and reviews that deal with all aspects of clinical and experimental neuropathology and related fields of neuroscience research. The scope of journal includes surgical and experimental pathomorphology, ultrastructure, immunohistochemistry, biochemistry and molecular biology of the nervous tissue. Papers on surgical neuropathology and neuroimaging are also welcome. The reports in other fields relevant to the understanding of human neuropathology might be considered.