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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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Star power: harnessing the reactive astrocyte response to promote remyelination in multiple sclerosis

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Neural Regeneration Research 2024年第3期19卷 578-582页

作者： Markley Silva Oliveira Junior Laura Reiche Emerson Daniele Ines Kortebi Maryam Faiz Patrick Küry Department of Neurology Neuroregeneration laboratoryMedical FacultyHeinrich-Heine-UniversityDüsseldorfGermany Institute of Medical Science University of TorontoTorontoCanada Division of Anatomy Department of SurgeryUniversity of TorontoTorontoCanada

Astrocytes are indispensable for central nervous system development and homeostasis.In response to injury and disease,astrocytes are integral to the immunological-and the,albeit limited,repair response.In this review,we will examine some of the functions reactive astrocytes play in the context of multiple sclerosis and related animal models.We will consider the heterogeneity or plasticity of astrocytes and the mechanisms by which they promote or mitigate demyelination.Finally,we will discuss a set of biomedical strategies that can stimulate astrocytes in their promyelinating response.

关键词： astrocytes demyelination drug-based therapies myelin repair oligodendrocyte precursor cells reactive astrogliosis

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SHP-2 promotes the maturation of oligodendrocyte precursor cells through Akt and ERKl/2 signaling in vitro

SHP-2 promotes the maturation of oligodendrocyte precursor c...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Xiu-Jie LIU,Yuan-Yuan LI,Yong ZHANG,Yan LU,Wei GUO,Peng LIU,Jia-Zhen ZHOU,Zheng-Hua XIANG, Cheng HE~* Institute of Neuroscience and Key Laboratory of Molecular Neurobiology of Ministry of Education,Second Military Medical University,Shanghai 200433,China

＜正＞Objective oligodendrocyte precursor cells（OPCs）differentiate into oligodendrocytes（OLs）,which are responsible for myelination.However,the molecular mechanisms of maturation and myelination by oligodendrocytes remain elusive.The present study is aim to explore the roles of SHP-2 in oligodendrocytes maturation.Methods In this study,we first searched the potential tyrosine phosphatases involved in oligodendrocytes maturation using OPCs as the model.Then,we characterized SHP-2 expression during the development of oligodendrocytes by RTPCR, immunostaining and Western blot.The roles of SHP-2 in olidendrocytes maturation were detected by gene manipulations subsequently.Finally,the mechanism was examined by detecting activities of concerned kinases. Results（1）We found that SHP-2 was persistently expressed during developmental process of oligodendrocytes.（2） SHP-2 knock down attenuated oligodendrocytes maturation and this effect was triiodo-L-thyronine（T3）dependent. Over-expression of SHP-2 promoted maturation in primary cultured oligodendrocytes.（3）It has been identified that SHP-2 may regulate oligodendrocytes maturation through Akt and Erkl/2 signaling.Conclusions SHP-2 promotes oligodendrocytes maturation via Akt and ERK1/2 signaling in vitro.

关键词： SHP-2 oligodendrocyte precursor cells maturation Akt ERK1/2

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Myt1L promotes the differentiation of oligodendrocyte precursor cells and accelerates remyelination in multiple sclerosis models

Myt1L promotes the differentiation of oligodendrocyte precur...

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中国神经科学学会第十二届全国学术会议

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 Second Military Medical University Wellcome Trust-Medical Research Council Stem Cell Institute University of Cambridge

Objective: The differentiation and maturation of oligodendrocyte precursor cells（OPCs） is essential for myelination and remyelination in CNS. The failure of OPCs to achieve terminal differentiation in demyelinating lesions often results in the unsuccessful remyelination in a variety of human demyelinating diseases. However, the molecular mechanisms controlling OPCs differentiation under pathological conditions remain largely unknown. Myt1L（myelin transcription factor 1-like）, mainly expressed in neurons, was associated with intellectual disability, schizophrenia or depression. In the present study, we have investigated the effect of Myt1L on OPCs differentiation and on the progress of LPC induced demyelination and subsequent remyelination. Methods: Firstly, we analyzed the expression pattern of Myt1L in CNS. Wecharacterized the expression pattern of Myt1L in oligodendrocyte lineage cells in vitro by immunocytofluorescence. To further explore the expression patterns of Myt1L during myelination in vivo, immunofluorescence staining of Myt1L in the white matter of mice from neonatal to adult was performed. In order to validate the expression pattern of Myt1L in the acute demyelination model in vivo, we constructed a model of LPC induced demyelination in mouse spinal cord. We also evaluated the regulation of Myt1L expression in oligodendrocyte lineage cells in LPC-model by immunofluorescence staining. Secondly, we evaluated the effects of Myt1L on oligodendrocytes maturation and myelination. To investigate the effect of Myt1L on OPCs differentiation in vitro, we transfected GFP-labeled Myt1L overexpressing viruses（Myt1L-OE） and Myt1L interfering viruses（Myt1L-RNAi） into cultured OPCs. Then we used q PCR, Western Blot and immunocytofluorescence to study the role of in OPCs differentiation. We also performed Brd U incorporation assay, Caspase3 staining analysis and Transwell assay to explore OPCs proliferation, apoptosis and migration. To define the effect of Myt1L on LPC-induced demyelination, lentivirus encoding Myt1L

关键词： Myt1L oligodendrocyte precursor cells Remyelination Demyelination Olig1

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oligodendrocyte pathology in fetal alcohol spectrum disorders

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Neural Regeneration Research 2022年第3期17卷 497-502页

作者： Nune Darbinian Michael E.Selzer Center for Neural Repair and Rehabilitation(Shriners Hospitals Pediatric Research Center) Lewis Katz School of Medicine at Temple UniversityPhiladelphiaPAUSA

The pathology of fetal alcohol syndrome and the less severe fetal alcohol spectrum disorders includes brain dysmyelination.Recent studies have shed light on the molecular mechanisms underlying these white matter abnormalities.Rodent models of fetal alcohol syndrome and human studies have shown suppressed oligodendrocyte differentiation and apoptosis of oligodendrocyte precursor cells.Ethanol exposure led to reduced expression of myelin basic protein and delayed myelin basic protein expression in rat and mouse models of fetal alcohol syndrome and in human histopathological specimens.Several studies have reported increased expression of many chemokines in dysmyelinating disorders in central nervous system,including multiple sclerosis and fetal alcohol syndrome.Acute ethanol exposure reduced levels of the neuroprotective insulin-like growth factor-1 in fetal and maternal sheep and in human fetal brain tissues,while ethanol increased the expression of tumor necrosis factor α in mouse and human neurons.White matter lesions have been induced in the developing sheep brain by alcohol exposure in early gestation.Rat fetal alcohol syndrome models have shown reduced axon diameters,with thinner myelin sheaths,as well as reduced numbers of oligodendrocytes,which were also morphologically aberrant oligodendrocytes.Expressions of markers for mature myelination,including myelin basic protein,also were reduced.The accumulating knowledge concerning the mechanisms of ethanol-induced dysmyelination could lead to the development of strategies to prevent dysmyelination in children exposed to ethanol during fetal development.Future studies using fetal oligodendrocyte-and oligodendrocyte precursor cell-derived exosomes isolated from the mother's blood may identify biomarkers for fetal alcohol syndrome and even implicate epigenetic changes in early development that affect oligodendrocyte precursor cell and oligodendrocyte function in adulthood.By combining various imaging modalities with molecular studies,it may be possible to determine

关键词： alcohol development dysmyelination ethanol fetal alcohol syndrome fetal brain myelin basic protein neurodegeneration oligodendrocyte injury oligodendrocyte precursor cells

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Neuroprotection and neuroregeneration:roles for the white matter

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Neural Regeneration Research 2022年第11期17卷 2376-2380页

作者： Vito Antonio Baldassarro Agnese Stanzani Luciana Giardino Laura Calzà Luca Lorenzini Department of Veterinary Medical Science University of BolognaBolognaItaly Interdepartmental Center for Industrial Research in Life Sciences and Technologies University of BolognaBolognaItaly Fondazione IRET Ozzano EmiliaItaly Department of Pharmacy and Biotechnology University of BolognaBolognaItaly Montecatone Rehabilitation Institute ImolaItaly

Efficient strategies for neuroprotection and repair are still an unmet medical need for neurodegenerative diseases and lesions of the central nervous system.Over the last few decades,a great deal of attention has been focused on white matter as a potential therapeutic target,mainly due to the discovery of the oligodendrocyte precursor cells in the adult central nervous system,a cell type able to fully repair myelin damage,and to the development of advanced imaging techniques to visualize and measure white matter lesions.The combination of these two events has greatly increased the body of research into white matter alte rations in central nervous system lesions and neurodegenerative diseases and has identified the oligodendrocyte precursor cell as a putative target for white matter lesion repair,thus indirectly contributing to neuroprotection.This review aims to discuss the potential of white matter as a therapeutic target for neuroprotection in lesions and diseases of the central nervous system.Pivot conditions are discussed,specifically multiple scle rosis as a white matter disease;spinal cord injury,the acute lesion of a central nervous system component where white matter prevails over the gray matte r,and Alzheimer's disease,where the white matter was considered an ancilla ry component until recently.We first describe oligodendrocyte precursor cell biology and developmental myelination,and its regulation by thyroid hormones,then briefly describe white matter imaging techniques,which are providing information on white matter involvement in central nervous system lesions and degenerative diseases.Finally,we discuss pathological mechanisms which interfere with myelin repair in adulthood.

关键词： Alzheimer's disease multiple sclerosis oligodendrocyte precursor cells spinal cord injury thyroid hormone traumatic brain injury white matter white matter imaging

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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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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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Expression and regulation of versican in neural precursor cells and their lineages

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Acta Pharmacologica Sinica 2007年第10期28卷 1519-1530页

作者： Wen-li GU~(2,3),Sai-li FU~2,Yan-xia WANG~2,Ying LI~2,Xiao-fei WANG~2,Xiao-ming XU~(2,4),Pei-hua LU~(2,5)~2 Department of Neurobiology,Shanghai Jiao Tong University School of Medicine,Shanghai 200025,China ~3 Department of ClinicalLaboratory,Ninth People's Hospital of Shanghai,Shanghai Jiao Tong University,Shanghai 200011,China ~4 Department of Neurological Surgery,University of Louisville School of Medicine,Louisville,Kentucky 40292,USA Department of Neurobiology Shanghai Jiao Tong University School of Medicine Shanghai China Department of Clinical Laboratory Ninth People's Hospital of Shanghai Shanghai Jiao Tong University Shanghai China Department of Neurological Surgery University of Louisville School of Medicine Louisville USA

Aim:To have a better understanding of the expression and regulation of versicanisoforms in neural precursor cells (NPC) and oligodendrogliogenesis.Methods:By immunocytochemistry,RT-PCR,and real-time PCR,we examined the tem-poral expression of versican in NPC isolated from embryonic d 16 rats as wellas in oligodendrocyte (OL) lineage cells induced to differentiate from NPC,which mimicked the oligodendrogliogenesis in vivo.Results:We found thatversican was constitutively expressed in NPC and their lineage cells,includingneurons,astrocytes,and OL.In addition,2 versican isoforms,V1/V0 and V2,were found to express at low levels in NPC,but at significantly higher levels inOL lineage cells.The peak expression of versican V2 was found at the oligo-dendrocyte precursor cell stage.Furthermore,the treatment of 2 pro-inflam-matory cytokines,TNF-α and IFN-γ,enhanced the transcription of versican V2in NPC in a dose-dependent manner,but showed no effect on V1/V0 expression.Conclusion:Taken together,our results demonstrate that versican,particularlythe inhibitory V2 isoform,is increasingly expressed in OL lineage cells inducedto differentiate from NPC.An increase in versican V2 expression after cytokinestimulation implies the interplay between the injury-induced upregulation ofinflammatory cytokines and chondroitin sulfate proteoglycan-mediated inhibi-tion of axonal regeneration after central nervous system injury.

关键词： chondroitin sulfate proteoglycans neural precursor cells oligodendrocyte precursor cells oligodendrocytes pro-inflammatory cytokines versican

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Effect of type-2 astrocytes on the viability of dorsal root ganglion neurons and length of neuronal processes

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Neural Regeneration Research 2014年第2期9卷 119-128页

作者： Chunling Fan Hui Wang Dan Chen Xiaoxin Cheng Kun Xiong Xuegang Luo Qilin Cao Department of Human Anatomy and Neurobiology Xiangya School of MedicineCentral South University The Vivian L Smith Department of Neurosurgery UT Medical School at Houston

The role of type-2 astrocytes in the repair of central nervous system injury remains poorly un- derstood. In this study, using a relatively simple culture condition in vitro, type-2 astrocytes, differentiated from oligodendrocyte precursor cells by induction with bone morphogenetic pro- tein-4, were co-cultured with dorsal root ganglion neurons. We examined the effects of type-2 astrocytes differentiated from oligodendrocyte precursor cells on the survival and growth of dorsal root ganglion neurons. Results demonstrated that the number of dorsal root ganglion neurons was higher following co-culture of oligodendrocyte precursor cells and type-2 astrocytes than when cultured alone, but lower than that of neurons co-cultured with type-1 astrocytes. The length of the longest process and the length of all processes of a single neuron were shortest in neurons cultured alone, followed by neurons co-cultured with type-2 astroc^es, then neurons co-cultured with oligodendrocyte precursor cells, and longest in neurons co-cultured with type-1 astrocytes. These results indicate that co-culture with type-2 astrocytes can increase neuronal survival rate and process length. However, compared with type-1 astrocytes and oligodendrocyte precursor cells, the promotion effects of type-2 astrocytes on the growth of dorsal root ganglion neurons were weaker.

关键词： nerve regeneration spinal cord injury oligodendrocyte oligodendrocyte precursor cells astrocytes bone morphogenetic protein neurons neurites dorsal root ganglion NIH grant neuralregeneration

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