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FTO alleviates cerebral ischemia/reperfusion-induced neuroinflammation by decreasing cGAS mRNA stability in an m6A-dependent manner

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收录情况： ◇ SCIE

作者：
Yu Zhiyong[1] * ; Zheng Linbo[1,2] * ; Geng Yan[1] * ; Zhang Yuting[1] ; Wang Yupeng[1] ; You Guoxing[1] ; Cai Mingsheng[3,6] ; Li Meili[3,5,6,*1] ; Cheng Xiao[4,7,8,*1] ; Zan Jie[1,*1] ;
机构： [1]School of Biomedical and Pharmaceutical sciences, Guangdong University of Technology, Guangzhou 510006, China [2]Department of Traditional Chinese Medicine, Guangdong Second Provincial General Hospital, Guangzhou 510310, China [3]Department of Laboratory Medicine, The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People’s Hospital, State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Qingyuan 511518, Guangdong, China [4]State Key Laboratory of Dampness Syndrome of Chinese Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangdong, China [5]Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou 511436, Guangzhou, China [6]Department of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou 511436, Guangdong, China [7]Provincial Key Laboratory of Research on Emergency in TCM, Guangzhou, China [8]Department of Neurology, Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou 510120, China
出处：
DOI： 10.1016/j.cellsig.2023.110751
ISSN：

关键词： Cerebral ischemia and reperfusion injury N6-Methyladenosine Fat mass and obesity-associated protein Cyclic GMP-AMP synthase Inflammation

摘要：
Microglia-mediated inflammation is a major contributor to the brain damage in cerebral ischemia and reperfusion (I/R) injury, and N6-Methyladenosine (m6A) has been implicated in cerebral I/R injury. Here, we explored whether m6A modification is associated with microglia-mediated inflammation in cerebral I/R injury and its underlying regulatory mechanism using an in vivo mice model of intraluminal middle cerebral artery occlusion/reperfusion (MCAO/R) and in vitro models of primary isolated microglia and BV2 microglial cells subjected to oxygen-glucose deprivation and reoxygenation (OGD/R) were used. We found microglial m6A modification increased and microglial fat mass and obesity-associated protein (FTO) expression decreased in cerebral I/R injury in vivo and in vitro. Inhibition of m6A modification by intraperitoneal injection of Cycloleucine (Cyc) in vivo or transfection of FTO plasmid in vitro significantly alleviated brain injury and microglia-mediated inflammatory response. Through Methylated RNA immunoprecipitation sequencing (MeRIP-Seq), RNA sequencing (RNA-Seq) and western blotting, we found that m6A modification promoted cerebral I/R-induced microglial inflammation via increasing cGAS mRNA stability to aggravate Sting/NF-κB signaling. In conclusion, this study deepens our understanding on the relationship of m6A modification and microglia-mediated inflammation in cerebral I/R injury, and insights a novel m6A-based therapeutic for inhibiting inflammatory response against ischemic stroke.Copyright © 2023. Published by Elsevier Inc.

基金：
This study was supported by the Science and Technology Planning Project of Guangzhou (202201010966), Guangdong Bureau of Traditional Chinese Medicine Project (20231017), Guangdong Provincial Key Laboratory of Research on Emergency in TCM (2017B030314176), the Natural Science Foundation of Guangdong Province (2022A1515012408 and 2021A1515012431), the Open Project of State Key Laboratory of Respiratory Disease (SKLRD-OP-202202, SKLRD-OP- 202317, and SKLRD-OP-202318), the Open Research Funds from the Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People’s Hospital (202301-204) and the National Natural Science Foundation of China (82272326).
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外文
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PubmedID：
中科院(CAS)分区：
出版当年[2022]版：
大类 | 2 区 生物学
小类 | 3 区 细胞生物学
最新[2025]版：
大类 | 2 区 生物学
小类 | 3 区 细胞生物学
JCR分区：
出版当年[2021]版：
Q2 CELL BIOLOGY
最新[2023]版：
Q2 CELL BIOLOGY

影响因子： 最新[2023版] 最新五年平均 出版当年[2021版] 出版当年五年平均 出版前一年[2020版] 出版后一年[2022版]

第一作者：
第一作者机构： [1]School of Biomedical and Pharmaceutical sciences, Guangdong University of Technology, Guangzhou 510006, China
共同第一作者：
通讯作者：
通讯机构： [1]School of Biomedical and Pharmaceutical sciences, Guangdong University of Technology, Guangzhou 510006, China [3]Department of Laboratory Medicine, The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People’s Hospital, State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Qingyuan 511518, Guangdong, China [4]State Key Laboratory of Dampness Syndrome of Chinese Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangdong, China [5]Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou 511436, Guangzhou, China [6]Department of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou 511436, Guangdong, China [7]Provincial Key Laboratory of Research on Emergency in TCM, Guangzhou, China [8]Department of Neurology, Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou 510120, China [*1]School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou 510006, China.
推荐引用方式(GB/T 7714)：
Yu Zhiyong,Zheng Linbo,Geng Yan,et al.FTO alleviates cerebral ischemia/reperfusion-induced neuroinflammation by decreasing cGAS mRNA stability in an m6A-dependent manner[J].CELLULAR SIGNALLING.2023,109:doi:10.1016/j.cellsig.2023.110751.
APA：
Yu Zhiyong,Zheng Linbo,Geng Yan,Zhang Yuting,Wang Yupeng...&Zan Jie.(2023).FTO alleviates cerebral ischemia/reperfusion-induced neuroinflammation by decreasing cGAS mRNA stability in an m6A-dependent manner.CELLULAR SIGNALLING,109,
MLA：
Yu Zhiyong,et al."FTO alleviates cerebral ischemia/reperfusion-induced neuroinflammation by decreasing cGAS mRNA stability in an m6A-dependent manner".CELLULAR SIGNALLING 109.(2023)

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