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Lipocalin-2-Mediated Insufficient Oligodendrocyte Progenitor Cell remyelination for White Matter Injury After Subarachnoid Hemorrhage via SCL22A17 Receptor/Early Growth Response Protein 1 Signaling

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Neuroscience Bulletin 2022年第12期38卷 1457-1475页

作者： Qiang Li Xufang Ru Yang Yang Hengli Zhao Jie Qu Weixiang Chen Pengyu Pan Huaizhen Ruan Chaojun Li Yujie Chen Hua Feng Department of Neurosurgery and State Key Laboratory of Trauma Burn and Combined InjurySouthwest HospitalThird Military Medical University(Army Medical University)Chongqing 400038China Department of Neurobiology College of Basic Medical SciencesThird Military Medical University(Army Medical University)Chongqing 400038China Model Animal Research Center Nanjing UniversityNanjing 210032China Chongqing Key Laboratory of Precision Neuromedicine and Neuroregenaration Southwest HospitalThird Military Medical University(Army Medical University)Chongqing 400038China Chongqing Clinical Research Center for Neurosurgery Southwest HospitalThird Military Medical University(Army Medical University)Chongqing 400038China

Insufficient remyelination due to impaired oligodendrocyte precursor cell(OPC)differentiation and maturation is strongly associated with irreversible white matter injury(WMI)and neurological deficits.We analyzed whole transcriptome expression to elucidate the potential role and underlying mechanism of action of lipocalin-2(LCN2)in OPC differentiation and WMI and identified the receptor SCL22A17 and downstream transcription factor early growth response protein 1(EGR1)as the key signals contributing to LCN2-mediated insufficient OPC remyelination.In LCN-knockdown and OPC EGR1 conditional-knockout mice,we discovered enhanced OPC differentiation in developing and injured white matter(WM);consistent with this,the specific inactivation of LCN2/SCl22A17/EGR1 signaling promoted remyelination and neurological recovery in both atypical,acute WMI due to subarachnoid hemorrhage and typical,chronic WMI due to multiple sclerosis.This potentially represents a novel strategy to enhance differentiation and remyelination in patients with white matter injury.

关键词： White matter injury Oligodendrocyte progenitor cell remyelination Subarachnoid hemorrhage Multiple sclerosis Lipocalin-2 Early growth response protein 1

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MFG-E8 Alleviates Cognitive Impairments Induced by Chronic Cerebral Hypoperfusion by Phagocytosing Myelin Debris and Promoting remyelination

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NEUROSCIENCE BULLETIN 2024年第4期40卷 483-499页

作者： Dong, Xiaohong Zhang, Zhi Shu, Xin Zhuang, Zi Liu, Pinyi Liu, Renyuan Xia, Shengnan Bao, Xinyu Xu, Yun Chen, Yan Nanjing Univ Nanjing Drum Tower Hosp Affiliated Hosp Dept NeurolMed Sch Nanjing 210008 Peoples R China Nanjing Univ Chinese Med Nanjing Drum Tower Hosp Dept Neurol Clin Coll Tradit Chinese & Western Med Nanjing 210008 Peoples R China Nanjing Univ Jiangsu Key Lab Mol Med Med Sch Nanjing 210008 Peoples R China Jiangsu Prov Key Discipline Neurol Nanjing 210008 Peoples R China Nanjing Med Univ Drum Tower Hosp Dept Neurol Nanjing 210008 Peoples R China

Chronic cerebral hypoperfusion is one of the pathophysiological mechanisms contributing to cognitive decline by causing white matter injury. Microglia phagocytosing myelin debris in a timely manner can promote remyelination and contribute to the repair of white matter. However, milk fat globule-epidermal growth factor-factor 8 (MFG-E8), a microglial phagocytosis-related protein, has not been well studied in hypoperfusion-related cognitive dysfunction. We found that the expression of MFG-E8 was significantly decreased in the brain of mice after bilateral carotid artery stenosis (BCAS). MFG-E8 knockout mice demonstrated more severe BCAS-induced cognitive impairments in the behavioral tests. In addition, we discovered that the deletion of MFG-E8 aggravated white matter damage and the destruction of myelin microstructure through fluorescent staining and electron microscopy. Meanwhile, MFG-E8 overexpression by AAV improved white matter injury and increased the number of mature oligodendrocytes after BCAS. Moreover, in vitro and in vivo experiments showed that MFG-E8 could enhance the phagocytic function of microglia via the alpha V beta 3/alpha V beta 5/Rac1 pathway and IGF-1 production to promote the differentiation of oligodendrocyte progenitor cells into mature oligodendrocytes. Interestingly, we found that MFG-E8 was mainly derived from astrocytes, not microglia. Our findings suggest that MFG-E8 is a potential therapeutic target for cognitive impairments following cerebral hypoperfusion.

关键词： White matter injury Cognitive dysfunction MFG-E8 remyelination Microglial phagocytosis WHITE-MATTER HYPERINTENSITIES NEURONAL DEATH ACTIVATION MICROGLIA TRANSDUCTION INTEGRIN LESIONS LIGAND MRI

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Decellularized optic nerve functional scaffold transplant facilitates directional axon regeneration and remyelination in the injured white matter of the rat spinal cord

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Neural Regeneration Research 2021年第11期16卷 2276-2283页

作者： Yu-Rong Bai Bi-Qin Lai Wei-Tao Han Jia-Hui Sun Ge Li Ying Ding Xiang Zeng Yuan-Huan Ma Yuan-Shan Zeng Key Laboratory for Stem Cells and Tissue Engineering Ministry of EducationSun Yat-sen UniversityGuangzhouGuangdong ProvinceChina Department of Histology and Embryology Zhongshan School of MedicineSun Yat-sen UniversityGuangzhouGuangdong ProvinceChina Co-innovation Center of Neuroregeneration Nantong UniversityNantongJiangsu ProvinceChina Institute of Spinal Cord Injury Sun Yat-sen UniversityGuangzhouGuangdong ProvinceChina Guangdong Provincial Key Laboratory of Brain Function and Disease Zhongshan School of MedicineSun Yat-sen UniversityGuangzhouGuangdong ProvinceChina

Axon regeneration and remyelination of the damaged region is the most common repair strategy for spinal cord injury.However,achieving good outcome remains difficult.Our previous study showed that porcine decellularized optic nerve better mimics the extracellular matrix of the embryonic porcine optic nerve and promotes the directional growth of dorsal root ganglion neurites.However,it has not been reported whether this material promotes axonal regeneration in vivo.In the present study,a porcine decellularized optic nerve was seeded with neurotrophin-3-overexpressing Schwann cells.This functional scaffold promoted the directional growth and remyelination of regenerating axons.In vitro,the porcine decellularized optic nerve contained many straight,longitudinal channels with a uniform distribution,and microscopic pores were present in the channel wall.The spatial micro topological structure and extracellular matrix were conducive to the adhesion,survival and migration of neural stem cells.The scaffold promoted the directional growth of dorsal root ganglion neurites,and showed strong potential for myelin regeneration.Furthermore,we transplanted the porcine decellularized optic nerve containing neurotrophin-3-overexpressing Schwann cells in a rat model of T10 spinal cord defect in vivo.Four weeks later,the regenerating axons grew straight,the myelin sheath in the injured/transplanted area recovered its structure,and simultaneously,the number of inflammatory cells and the expression of chondroitin sulfate proteoglycans were reduced.Together,these findings suggest that porcine decellularized optic nerve loaded with Schwann cells overexpressing neurotrophin-3 promotes the directional growth of regenerating spinal cord axons as well as myelin regeneration.All procedures involving animals were conducted in accordance with the ethical standards of the Institutional Animal Care and Use Committee of Sun Yat-sen University(approval No.SYSU-IACUC-2019-B034)on February 28,2019.

关键词： axonal regeneration decellularized optic nerve directional regeneration functional scaffold microenvironment neurotrophin-3 optic nerve remyelination Schwann cells tissue engineering white matter injury

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Dynamic glial response and crosstalk in demyelination-remyelination and neurodegeneration processes

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Neural Regeneration Research 2021年第7期16卷 1359-1368页

作者： Tianci Chu Lisa B.E.Shields Wenxin Zeng Yi Ping Zhang Yuanyi Wang Gregory N.Barnes Christopher B.Shields Jun Cai Pediatric Research Institute Department of PediatricsUniversity of Louisville School of MedicineLouisvilleKYUSA Norton Neuroscience Institute Norton HealthcareLouisvilleKYUSA Department of Spine Surgery The First Hospital of Jilin UniversityChangchunJilin ProvinceChina Department of Neurology University of Louisville School of MedicineLouisvilleKYUSA Department of Pharmacology and Toxicology University of LouisvilleLouisvilleKYUSA Department of Neurological Surgery University of Louisville School of MedicineLouisvilleKYUSA

Multiple sclerosis is an autoimmune disease in which the immune system attacks the myelin sheath in the central nervous system.It is characterized by blood-brain barrier dysfunction throughout the course of multiple sclerosis, followed by the entry of immune cells and activation of local microglia and astrocytes.Glial cells(microglia, astrocytes, and oligodendrocyte lineage cells) are known as the important mediators of neuroinflammation, all of which play major roles in the pathogenesis of multiple sclerosis.Network communications between glial cells affect the activities of oligodendrocyte lineage cells and influence the demyelination-remyelination process.A finely balanced glial response may create a favorable lesion environment for efficient remyelination and neuroregeneration.This review focuses on glial response and neurodegeneration based on the findings from multiple sclerosis and major rodent demyelination models.In particular, glial interaction and molecular crosstalk are discussed to provide insights into the potential cell-and molecule-specific therapeutic targets to improve remyelination and neuroregeneration.

关键词： astrocyte crosstalk demyelination glial response microglia/macrophage multiple sclerosis neurodegeneration neuroinflammation oligodendrocyte lineage cells remyelination

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Conditional Deletion of Foxg1 Alleviates Demyelination and Facilitates remyelination via the Wnt Signaling Pathway in Cuprizone-Induced Demyelinated Mice

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Neuroscience Bulletin 2021年第1期37卷 15-30页

作者： Fuxing Dong Dajin Liu Feiyu Jiang Yaping Liu Xiuxiang Wu Xuebin Qu Jing Liu Yan Chen Hongbin Fan Ruiqin Yao Department of Cell Biology and Neurobiology Xuzhou Key Laboratory of NeurobiologyJiangsu Key Laboratory of New Drug Research and Clinical PharmacyXuzhou Medical UniversityXuzhou 221004China Public Experimental Research Center Xuzhou Medical UniversityXuzhou 221004China Department of Neurology Affiliated Hospital of Xuzhou Medical UniversityXuzhou 221006China

The massive loss of oligodendrocytes caused by various pathological factors is a basic feature of many demyelinating diseases of the central nervous system(CNS). Based on a variety of studies, it is now well established that impairment of oligodendrocyte precursor cells(OPCs) to differentiate and remyelinate axons is a vital event in the failed treatment of demyelinating diseases. Recent evidence suggests that Foxg1 is essential for the proliferation of certain precursors and inhibits premature neurogenesis during brain development. To date, very little attention has been paid to the role of Foxg1 in the proliferation and differentiation of OPCs in demyelinating diseases of the CNS. Here, for the first time, we examined the effects of Foxg1 on demyelination and remyelination in the brain using a cuprizone(CPZ)-induced mouse model. In this work, 7-week-old Foxg1 conditional knockout and wild-type(WT) mice were fed a diet containing 0.2% CPZ w/w for 5 weeks, after which CPZ was withdrawn to enable remyelination. Our results demonstrated that, compared with WT mice, Foxg1-knockout mice exhibited not only alleviated demyelination but also accelerated remyelination of the demyelinated corpus callosum. Furthermore, we found that Foxg1 knockout decreased the proliferation of OPCs and accelerated their differentiation into mature oligodendrocytes both in vivo and in vitro. Wnt signaling plays a critical role in development and in a variety of diseases. GSK-3 b, a key regulatory kinase in the Wnt pathway, regulates the ability of b-catenin to enter nuclei, where it activates the expression of Wnt target genes. We then used SB216763,a selective inhibitor of GSK-3 b activity, to further demonstrate the regulatory mechanism by which Foxg1 affects OPCs in vitro. The results showed that SB216763 clearly inhibited the expression of GSK-3 b, which abolished the effect of the proliferation and differentiation of OPCs caused by the knockdown of Foxg1. These results suggest that Foxg1 is involved in the proliferation and differenti

关键词： Foxg1 Oligodendrocyte precursor cells Demyelination remyelination Wnt

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Rosmarinic acid ameliorates hypoxia/ischemia induced cognitive deficits and promotes remyelination

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Neural Regeneration Research 2020年第5期15卷 894-902页

作者： Man Li Miao-Miao Cui Nwobodo Alexander Kenechukwu Yi-Wei Gu Yu-Lin Chen Si-Jing Zhong Yu-Ting Gao Xue-Yan Cao Li Wang Fu-Min Liu Xiang-Ru Wen Department of Genetics Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina Department of Urology the First Affiliated Hospital of Harbin Medical UniversityHarbinHeilongjiang ProvinceChina Xuzhou Medical University Clinical Medical College XuzhouJiangsu ProvinceChina Department of Clinical Laboratory Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina Research Center for Neurobiology and Department of Neurobiology Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina

Rosmarinic acid,a common ester extracted from Rosemary,Perilla frutescens,and Salvia miltiorrhiza Bunge,has been shown to have protective effects against various diseases.This is an investigation into whether rosmarinic acid can also affect the changes of white matter fibers and cognitive deficits caused by hypoxic injury.The right common carotid artery of 3-day-old rats was ligated for 2 hours.The rats were then prewarmed in a plastic container with holes in the lid,which was placed in 37°C water bath for 30 minutes.Afterwards,the rats were exposed to an atmosphere with 8% O2 and 92% N2 for 30 minutes to establish the perinatal hypoxia/ischemia injury models.The rat models were intraperitoneally injected with rosmarinic acid 20 mg/kg for 5 consecutive days.At 22 days after birth,rosmarinic acid was found to improve motor,anxiety,learning and spatial memory impairments induced by hypoxia/ischemia injury.Furthermore,rosmarinic acid promoted the proliferation of oligodendrocyte progenitor cells in the subventricular zone.After hypoxia/ischemia injury,rosmarinic acid reversed to some extent the downregulation of myelin basic protein and the loss of myelin sheath in the corpus callosum of white matter structure.Rosmarinic acid partially slowed down the expression of oligodendrocyte marker Olig2 and myelin basic protein and the increase of oligodendrocyte apoptosis marker inhibitors of DNA binding 2.These data indicate that rosmarinic acid ameliorated the cognitive dysfunction after perinatal hypoxia/ischemia injury by improving remyelination in corpus callosum.This study was approved by the Animal Experimental Ethics Committee of Xuzhou Medical University,China (approval No.20161636721) on September 16,2017.

关键词： cognitive dysfunction corpus callosum differentiation/DNA binding factor 2 hypoxia/ischemia myelin basic protein myelin sheath remyelination rosmarinic acid

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Pinocembrin Promotes OPC Differentiation and remyelination via the mTOR Signaling Pathway

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Neuroscience Bulletin 2021年第9期37卷 1314-1324页

作者： Qi Shao Ming Zhao Wenwen Pei Yingyan Pu Mingdong Liu Weili Liu Zhongwang Yu Kefu Chen Hong Liu Benqiang Deng Li Cao Institute of Neuroscience Key Laboratory of Molecular Neurobiology of the Ministry of Education and the Collaborative Innovation Center for Brain ScienceNaval Medical UniversityShanghai 200433China Changhai Stroke Center Changhai HospitalNaval Medical UniversityShanghai 200433China The 983rd Hospital of Joint Logistics Support Forces of the PLA Tianjin 300142China The 988th Hospital of Joint Logistics Support Forces of the PLA Zhengzhou 450000China

The exacerbation of progressive multiple sclerosis(MS)is closely associated with obstruction of the differentiation of oligodendrocyte progenitor cells(OPCs).To discover novel therapeutic compounds for enhancing remyelination by endogenous OPCs,we screened for myelin basic protein expression using cultured rat OPCs and a library of small-molecule compounds.One of the most effective drugs was pinocembrin,which remarkably promoted OPC differentiation and maturation without affecting cell proliferation and survival.Based on these in vitro effects,we further assessed the therapeutic effects of pinocembrin in animal models of demyelinating diseases.We demonstrated that pinocembrin significantly ameliorated the progression of experimental autoimmune encephalomyelitis(EAE)and enhanced the repair of demyelination in lysolectin-induced lesions.Further studies indicated that pinocembrin increased the phosphorylation level of mammalian target of rapamycin(mTOR).Taken together,our results demonstrated that pinocembrin promotes OPC differentiation and remyelination through the phosphorylated mTOR pathway,and suggest a novel therapeutic prospect for this natural flavonoid product in treating demyelinating diseases.

关键词： Pinocembrin Oligodendrocytes Differentiation remyelination MTOR

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Myt1L Promotes Differentiation of Oligodendrocyte Precursor Cells and is Necessary for remyelination After Lysolecithin-Induced Demyelination

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Neuroscience Bulletin 2018年第2期34卷 247-260页

作者： Yanqing Shi Qi Shao Zhenghao Li Ginez A. Gonzalez Fengfeng Lu Dan Wang Yingyan Pu Aijun Huang Chao Zhao Cheng He Li Cao Institute of Neuroscience Key Laboratory of Molecular Neurobiology of The Ministry of Education and The Collaborative Innovation Center for Brain Science Second Military Medical University Shanghai 200433 China Institute of Health Sciences Anhui University Hefei 230601China Wellcome Trust-Medical Research Council Stem Cell Insti-tute University of Cambridge Cambridge CB2 0AH UK

The differentiation and maturation of oligodendrocyte precursor cells(OPCs) is essential for myelination and remyelination in the CNS. The failure of OPCs to achieve terminal differentiation in demyelinating lesions often results in unsuccessful remyelination in a variety of human demyelinating diseases. However, the molecular mechanisms controlling OPC differentiation under pathological conditions remain largely unknown. Myt1 L(myelin transcription factor 1-like), mainly expressed in neurons,has been associated with intellectual disability, schizophrenia, and depression. In the present study, we found that Myt1 L was expressed in oligodendrocyte lineage cells during myelination and remyelination. The expression level of Myt1 L in neuron/glia antigen 2-positive(NG2+)OPCs was significantly higher than that in mature CC1+oligodendrocytes. In primary cultured OPCs,overexpression of Myt1 L promoted, while knockdown inhibited OPC differentiation. Moreover, Myt1 L was potently involved in promoting remyelination after lysolecithin-induced demyelination in vivo. Ch IP assays showed that Myt1 L bound to the promoter of Olig1 and transcriptionally regulated Olig1 expression. Taken together, our findings demonstrate that Myt1 L is an essential regulator of OPC differentiation, thereby supporting Myt1 L as a potential therapeutic target for demyelinating diseases.

关键词： Myt1L Oligodendrocyte precursor cells remyelination Demyelination Olig1

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Shikimic Acid Promotes Oligodendrocyte Precursor Cell Differentiation and Accelerates remyelination in Mice

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Neuroscience Bulletin 2019年第3期35卷 434-446页

作者： Fengfeng Lu Dou Yin Yingyan Pu Weili Liu Zhenghao Li Qi Shao Cheng He Li Cao Institute of Physical Science and Information Technology Anhui UniversityHefei 230601China Institute of Neuroscience Key Laboratory of Molecular Neurobiology of The Ministry of Educationand The Collaborative Innovation Center for Brain ScienceSecond Military Medical UniversityShanghai 200433China

The obstacle to successful remyelination in demyelinating diseases, such as multiple sclerosis, mainly lies in the inability of oligodendrocyte precursor cells(OPCs) to differentiate, since OPCs and oligodendrocytelineage cells that are unable to fully differentiate are found in the areas of demyelination. Thus, promoting the differentiation of OPCs is vital for the treatment of demyelinating diseases. Shikimic acid(SA) is mainly derived from star anise, and is reported to have antiinfluenza, anti-oxidation, and anti-tumor effects. In the present study, we found that SA significantly promoted the differentiation of cultured rat OPCs without affecting their proliferation and apoptosis. In mice, SA exerted therapeutic effects on experimental autoimmune encephalomyelitis(EAE), such as alleviating clinical EAE scores, inhibiting inflammation, and reducing demyelination in the CNS. SA also promoted the differentiation of OPCs as well as their remyelination after lysolecithin-induced demyelination.Furthermore, we showed that the promotion effect of SA on OPC differentiation was associated with the up-regulation of phosphorylated m TOR. Taken together, our resultsdemonstrated that SA could act as a potential drug candidate for the treatment of demyelinating diseases.

关键词： Shikimic acid Oligodendrocyte precursor cells Demyelination remyelination

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New ex vivo demyelination/remyelination models to defeat multiple sclerosis and neuromyelitis optica

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Neural Regeneration Research 2019年第10期14卷 1715-1716页

作者： Yiting Liu Department of Neurology School of Medicine University of Colorado

Multiple sclerosis (MS) and neuromyelitis optica (NMO) are inflammatory diseases of the central nervous system (CNS) resulting in CNS inflammation, infiltration of peripheral immune cells, loss of myelin and oligodendrocytes, interruption of axonal communication, and neurologic deficits. Following oligodendrocyte injury, newly generated myelinating oligodendrocytes derived from oligodendrocyte progenitors (OPCs) may produce new myelin sheaths around denuded axons (remyelination) restoring neuronal function (Verden and Macklin, 2016). While remyelination is apparent in MS lesions, the process is often inefficient;in NMO, remyelination is even more limited.

关键词： Multiple sclerosis(MS) inflammatory diseases remyelination is even more limited

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