{"title":"在脑卒中模型中，ZDHHC16通过抑制CREB促进神经细胞铁下垂。","authors":"Dongmei Xu, Hua Liu, Xiaoyu Deng, Jifan Fu","doi":"10.5114/fn.2024.145878","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>The present study explored the effects and possible mechanisms of ZDHHC16 in a model of cerebral apoplexy (CA).</p><p><strong>Material and methods: </strong>Patients with CA were collected from our hospital. Mice were used to establish an middle cerebral artery occlusion (MCAO) model.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusions: </strong>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.</p>","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":"{\"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\":\"<p><strong>Introduction: </strong>The present study explored the effects and possible mechanisms of ZDHHC16 in a model of cerebral apoplexy (CA).</p><p><strong>Material and methods: </strong>Patients with CA were collected from our hospital. Mice were used to establish an middle cerebral artery occlusion (MCAO) model.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusions: </strong>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.</p>\",\"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}","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}
ZDHHC16 promoted neurocyte ferroptosis by suppression of CREB in a cerebral apoplexy model.
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.
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.
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