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Glycolysis inhibition ameliorates brain injury after ischemic stroke by promoting the function of myeloid-derived suppressor cells.

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收录情况： ◇ SCIE

作者：
Yan Jingwei[1,2,3] * ; Li Anqi[1,2,3,4] * ; Chen Xianglin[1] * ; Cao Kaixiang[1,2,3] ; Song Mingchuan[1,2,3] ; Guo Shuai[1,2,3] ; Li Zou[1,2,3] ; Huang Shuqi[1,2,3] ; Li Ziling[1,2,3] ; Xu Danghan[5] ; Wang Yong[6] ; Dai Xiaoyan[7] ; Feng Du[1,2,3] ; Huo Yuqing[6] ; He Jun[5,*1] ; Xu Yiming[1,2,3,*2] ;
机构： [1]The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People’s Hospital, Guangzhou Medical University, Guangzhou, China [2]School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China [3]State Key Lab of Respiratory Disease, Guangzhou Medical University, Guangzhou, China [4]Department of Radiology, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China [5]Department of Rehabilitation Center, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China [6]College of Basic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China [7]Guangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, China [8]Vascular Biology Center, Medical College of Georgia, Augusta University, Augusta, GA, USA
出处：
DOI： 10.1016/j.phrs.2022.106208
ISSN：

摘要：
Myeloid-derived suppressor cells (MDSCs) are a heterogeneous population of immature myeloid cells which are immunosuppressive and glycolytically inactive in inflammatory diseases. However, it is unknown whether MDSCs contribute to ischemic stroke and how glycolysis regulates MDSC function in such a context. Here, we showed that MDSCs arise in the blood of patients at early phase of stroke. Similar results were observed in temporary middle cerebral artery occlusion-induced cerebral ischemic mice. Pharmaceutical exhaustion of MDSCs aggravated, while adoptive transfer of MDSCs rescued the ischemic brain injury. However, the differentiation of MDSCs into immunopotent myeloid cells which coincides with increased glycolysis was observed in the context of ischemic stroke. Mechanistically, the glycolytic product lactate autonomously induces MDSC differentiation through activation of mTORC1, and paracrinely activates Th1 and Th17 cells. Moreover, gene knockout or inhibition of the glycolytic enzyme PFKFB3 increased endogenous MDSCs by blocking their differentiation, and improved ischemic brain injury. Collectively, these results revealed that glycolytic switch decreases the immunosuppressive and neuroprotective role of MDSCs in ischemic stroke and pharmacological targeting MDSCs via glycolysis inhibition constitutes a promising therapeutic strategy for ischemic stroke.Copyright © 2022. Published by Elsevier Ltd.

基金：
This work was supported by grants from the Natural Science Foundation of China (Grant number: 81870217 and 81700395), the Key Project of Department of Education of Guangdong Province (Grant number: 2018KZDXM053), and American Heart Association (Grant number: 15POST22810024). The funders had no contribution to the study design, data collection and analysis, interpretation and writing of the manuscript.
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中科院(CAS)分区：
出版当年[2021]版：
大类 | 2 区 医学
小类 | 2 区 药学
最新[2025]版：
大类 | 2 区 医学
小类 | 1 区 药学
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出版当年[2020]版：
Q1 PHARMACOLOGY & PHARMACY
最新[2023]版：
Q1 PHARMACOLOGY & PHARMACY

影响因子： 最新[2023版] 最新五年平均 出版当年[2020版] 出版当年五年平均 出版前一年[2019版] 出版后一年[2021版]

第一作者：
第一作者机构： [1]The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People’s Hospital, Guangzhou Medical University, Guangzhou, China [2]School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China [3]State Key Lab of Respiratory Disease, Guangzhou Medical University, Guangzhou, China
共同第一作者：
通讯作者：
通讯机构： [1]The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People’s Hospital, Guangzhou Medical University, Guangzhou, China [2]School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China [3]State Key Lab of Respiratory Disease, Guangzhou Medical University, Guangzhou, China [5]Department of Rehabilitation Center, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China [*1]The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Jichang Road, Baiyun District, Guangzhou 510405, China [*2]School of Basic Medical Sciences, Guangzhou Medical University, Research Building, A1-628, Xinzao Road, Panyu District, Guangzhou 511400, China.
推荐引用方式(GB/T 7714)：
Yan Jingwei,Li Anqi,Chen Xianglin,et al.Glycolysis inhibition ameliorates brain injury after ischemic stroke by promoting the function of myeloid-derived suppressor cells.[J].PHARMACOLOGICAL RESEARCH.2022,179:doi:10.1016/j.phrs.2022.106208.
APA：
Yan Jingwei,Li Anqi,Chen Xianglin,Cao Kaixiang,Song Mingchuan...&Xu Yiming.(2022).Glycolysis inhibition ameliorates brain injury after ischemic stroke by promoting the function of myeloid-derived suppressor cells..PHARMACOLOGICAL RESEARCH,179,
MLA：
Yan Jingwei,et al."Glycolysis inhibition ameliorates brain injury after ischemic stroke by promoting the function of myeloid-derived suppressor cells.".PHARMACOLOGICAL RESEARCH 179.(2022)

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