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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： Xiaohong Dong Zhi Zhang Xin Shu Zi Zhuang Pinyi Liu Renyuan Liu Shengnan Xia Xinyu Bao Yun Xu Yan Chen Department of Neurology Nanjing Drum Tower HospitalAffiliated Hospital of Medical SchoolNanjing UniversityNanjing210008China Department of Neurology Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western MedicineNanjing University of Chinese MedicineNanjing210008China Department of Neurology Drum Tower Hospital of Nanjing Medical UniversityNanjing210008China Jiangsu Key Laboratory for Molecular Medicine Medical School of Nanjing UniversityNanjing210008China Jiangsu Provincial Key Discipline of Neurology Nanjing210008China

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 theαVβ3/αVβ5/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

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Activation of glutamatergic neurons in the somatosensory cortex promotes remyelination in ischemic vascular dementia

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Fundamental Research 2024年第1期4卷 188-198页

作者： Yi-Ting Zhou Da-Dao An Yi-Xin Xu Ying Zhou Qing-Qing Li Hai-Bin Dai Xiang-Nan Zhang Yi Wang Min Lou Zhong Chen Wei-Wei Hu Department of Pharmacology and Department of Pharmacy of the Second Affiliated Hospital NHC and CAMS Key Laboratory of Medical NeurobiologySchool of Basic Medical SciencesCollege of Pharmaceutical SciencesZhejiang University School of MedicineHangzhou 310058China Department of Pharmacy Sir Run Run Shaw HospitalHangzhou 310012China Key Laboratory of Neuropharmacology and Translational Medicine of Zhejiang Province School of Pharmaceutical SciencesZhejiang Chinese Medical UniversityHangzhou 310053China Department of Neurology the Second Affiliated Hospital of Zhejiang UniversitySchool of MedicineHangzhou 310003China

Chronic cerebral hypoperfusion can cause progressive demyelination as well as ischemic vascular dementia,however no effective treatments are available.Here,based on magnetic resonance imaging studies of patients with white matter damage,we found that this damage is associated with disorganized cortical structure.In a mouse model,optogenetic activation of glutamatergic neurons in the somatosensory cortex significantly promoted oligodendrocyte progenitor cell(OPC)proliferation,remyelination in the corpus callosum,and recovery of cognitive ability after cerebral hypoperfusion.The therapeutic effect of such stimulation was restricted to the upper layers of the cortex,but also spanned a wide time window after ischemia.Mechanistically,enhancement of glutamatergic neuron-OPC functional synaptic connections is required to achieve the protection effect of activating cortical glutamatergic neurons.Additionally,skin stroking,an easier method to translate into clinical practice,activated the somatosensory cortex,thereby promoting OPC proliferation,remyelination and cognitive recovery following cerebral hypoperfusion.In summary,we demonstrated that activating glutamatergic neurons in the somatosensory cortex promotes the proliferation of OPCs and remyelination to recover cognitive function after chronic cerebral hypoperfusion.It should be noted that this activation may provide new approaches for treating ischemic vascular dementia via the precise regulation of glutamatergic neuron-OPC circuits.

关键词： Chronic cerebral hypoperfusion Optogenetic stimulation Oligodendrocyte progenitor cellIschemic vascular dementia Glutamatergic neuron remyelination

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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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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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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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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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The mechanism of Naringin-enhanced remyelination after spinal cord injury

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Neural Regeneration Research 2017年第3期12卷 470-477页

作者： Wei Rong Yong-wei Pan Xu Cai Fei Song Zhe Zhao Song-hua Xiao Cheng Zhang Department of Orthopedics Beijing Tsinghua Changgung HospitalMedical CenterTsinghua UniversityBeijing Key Laboratory of Bioelectromagnetism Beijing Key Laboratory of Bioelectromagnetism Institute of Electrical EngineeringChinese Academy of Sciences

Our previous study revealed that intragastric administration of naringin improved remyelination in rats with spinal cord injury and promoted the recovery of neurological function of the injured spinal cord.This study sought to reveal the mechanisms by which naringin improves oligodendrocyte precursor cell differentiation and maturation,and promotes remyelination.Spinal cord injury was induced in rats by the weight-drop method.Naringin was intragastrically administered daily（20,40 mg/kg） for 4 weeks after spinal cord injury induction.Behavioral assessment,histopathological staining,immunofluorescence spectroscopy,ultrastructural analysis and biochemical assays were employed.Naringin treatment remarkably mitigated demyelination in the white matter,increased the quality of myelinated nerve fibers and myelin sheath thickness,promoted oligodendrocyte precursor cell differentiation by upregulating the expression of NKx2.2 and 2′3′-cyclic nucleotide 3′-phosphodiesterase,and inhibited β-catenin expression and glycogen synthase kinase-3β（GSK-3β） phosphorylation.These findings indicate that naringin treatment regulates oligodendrocyte precursor cell differentiation and promotes remyelination after spinal cord injury through the β-catenin/GSK-3β signaling pathway.

关键词： nerve regeneration spinal cord injury naringin remyelination oligodendrocyte precursor cells oligodendrocytes β-catenin glycogen synthase kinase-3β NKx2.2 2＇,3＇-cyclic nucleotide 3＇-phosphodiesterase behavioral assessment neural regeneration

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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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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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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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