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Rotarod training reverses corticosterone-induced motor deficits via oligodendrocyte lineage cell modulation 认领 引用
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作者 Jada Chia-Di Lee Benson Wui-Man Lau +6 位作者 Suk-Yu Yau Joseph Wai-Hin Leung Harmony Kai-Hei Wong Dalinda Isabel Sanchez Vidana Tatia M.C.Lee Wu-Tian Wu Kwok-Fai So 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第6期2440-2447,共8页
Adult-born oligodendrocytes are continuously produced in the brains of rodents.The functional role of these cells has been linked to the motor-related activities of healthy animals and is vital for acquiring new motor... Adult-born oligodendrocytes are continuously produced in the brains of rodents.The functional role of these cells has been linked to the motor-related activities of healthy animals and is vital for acquiring new motor skills.However,the relationship between these cells and the control of motor-related activities has not been investigated in pathological conditions.Therefore,the aim of this study is to investigate the role of oligodendrocytes in depression-related motor deficits and the effects of training.Psychomotor retardation is a key symptom of depression.Consistent with the impairments observed in rodent motor performance,the proliferation and activation of adult-born oligodendrocytes are altered in a corticosterone-induced stress paradigm.Therapeutic rotarod training can alleviate these symptoms by reversing the aforementioned changes.Notably,these alterations are particularly pronounced in layer I of the motor cortex.Thus,this study provides evidence of the potential functional involvement of adult-born oligodendrocytes in the motor impairments observed in the depressed animals.Additionally,it offers preliminary results for further investigation into layer I of the motor cortex in relation to these pathological conditions. 展开更多
关键词 corticosterone-induced stress exercise major depressive disorder motor cortex motor deficits motor training myelination oligodendrocyte lineage cells oligodendrocyte precursor cells psychomotor retardation
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Oligodendrocyte precursor cells in the substantia nigra:Implications for Parkinson’s disease 认领 引用
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作者 Julia C.Fitzgerald Friederike Pfeiffer 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第8期3551-3552,共2页
Current evidence for oligodendrocyte precursor cell involvement in Parkinson’s disease:Oligodendroglial cells comprise a large cell population in the substantia nigra(SN).We recently reported a stable portion of olig... Current evidence for oligodendrocyte precursor cell involvement in Parkinson’s disease:Oligodendroglial cells comprise a large cell population in the substantia nigra(SN).We recently reported a stable portion of oligodendrocyte precursor cells(OPCs)in the SN pars compacta(SNpc)in a 1:1 ratio with dopaminergic neurons:15%of cells in neonate and young mice,rising to 20%in aged mice.Moreover,this portion represents only 45%of all oligodendroglial cells in the SNpc and 54%of all oligodendroglial cells in the SN pars reticulata(SNpr)(Fitzgerald et al.,2025).The SN is a deeply located area of the midbrain and the site of dopaminergic degeneration in Parkinson’s disease(PD).Recent advancement of single-cell transcriptomics revealed the involvement of non-neuronal cells in PD,with PD risk variants being strongly associated with oligodendroglia(reviewed by Salazar Campos et al.,2025). 展开更多
关键词 oligodendrocyte precursor cell oligodendrocyte precursor cells opcs substantia nigra sn we pars compacta snpc Parkinson's disease dopaminergic neurons oligodendroglial cells substantia nigra
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Oligodendrocyte precursor cell-neuronal lysosomal pathway:A novel therapeutic target for neurodegenerative diseases 认领 引用
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作者 Li-Pao Fang Yibo Zhao Xianshu Bai 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第6期2355-2356,共2页
Oligodendrocyte precursor cells(OPCs)tile the central nervous system ubiquitously,accounting for about 5%of the total cell population in the central nervous system.Beyond their role in myelination,OPCs actively shape ... Oligodendrocyte precursor cells(OPCs)tile the central nervous system ubiquitously,accounting for about 5%of the total cell population in the central nervous system.Beyond their role in myelination,OPCs actively shape neural circuits(Fang and Bai,2023),by releasing neuromodulators,pruning synapses,maintaining the homeostasis of extracellular potassium concentration,and interacting with endothelial cells. 展开更多
关键词 oligodendrocyte precursor cells opcs tile neuromodulatorspruning synapsesmaintaining oligodendrocyte precursor cells endothelial cells neuronal lysosomal pathway extracellular potassium central nervous systembeyond shape neural circuits fang
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Hippocampal Oligodendrocytes Regulate Mossy Fiber Development Involved in Epileptic Responses 认领 引用
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作者 Chunxia Jiang Yunan Hu +2 位作者 Feng Zhang Mengsheng Qiu Xiaofeng Zhao 《Neuroscience Bulletin》 SCIE CAS CSCD 2026年第4期781-794,共14页
Although oligodendrocytes(OLs)are known to form the myelin sheath around neuronal axons for the saltatory conduction of action potentials,recent studies have suggested that OLs also modulate neuronal function and plas... Although oligodendrocytes(OLs)are known to form the myelin sheath around neuronal axons for the saltatory conduction of action potentials,recent studies have suggested that OLs also modulate neuronal function and plasticity.In the present study,we found that OL maturation deficiency in Myrf-CKO mice caused spontaneous epileptogenesis and resulted in death.To further investigate the association between OL development and epilepsy,we examined the Adamts4 KO mouse line,which has a mild OL differentiation phenotype in the hippocampus.As a result,the differentiation defect in the mutant hippocampus reduced the expression of myelin-associated glycoprotein and lessened its inhibition of the dephosphorylation of phosphorylated tropomyosin-related kinase B,which is associated with retarded adolescent hippocampal mossy fiber development and higher susceptibility to epileptogenesis in adulthood.More importantly,enhancing differentiation by orally administered clemastine rescues the defective mossy fiber development in the early postnatal period and attenuates epilepsy susceptibility in adults.Together,these results strongly suggest that an OL differentiation defect in the hippocampus may contribute to susceptibility to epilepsy in adults. 展开更多
关键词 Oligodendrocyte Diferentiation Myelinassociated glycoprotein Tropomyosin-related kinase B Epilepsy
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HNRNPH2 variant linked to intellectual disability disrupts myelination by impairing oligodendrocyte differentiation 认领 引用
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作者 Yang Jiao Xingyu Pan +12 位作者 Jingrong Zhao Xiaoyu Teng Xiaoyi Liao Xinyu Hu Qiu Wang Dandan Zheng Yuxiang Pan Xiaohui Deng Xinyi Tan Yun Stone Shi Xu Zhang Lan Bao Bin Wang 《Journal of Genetics and Genomics》 SCIE CAS CSCD 2026年第5期854-867,共14页
Intellectual disability(ID)arises from complex pathogenic mechanisms.Although myelin dysfunction and white matter damage have been implicated,the cellular and molecular mechanisms linking impaired myelination to cogni... Intellectual disability(ID)arises from complex pathogenic mechanisms.Although myelin dysfunction and white matter damage have been implicated,the cellular and molecular mechanisms linking impaired myelination to cognitive deficits remain largely unknown.Here,we identify a de novo heterogeneous nuclear ribonucleoprotein H2(HNRNPH2)variant,c.638C>T(p.Pro213Leu),in patients with ID.The Hnrnph2P213L knock-in mice display spatial learning deficits,representing a partial phenotypic overlap with HNRNPH2-related neurodevelopmental disorder.Notably,Hnrnph2P213L mice exhibit significant myelination defects,primarily due to the impaired differentiation of oligodendrocyte progenitor cells.Furthermore,the myelin-enhancing drug benztropine rescues myelination,restores myelin-related gene expression,and ameliorates cognitive deficits,highlighting the role of hnRNPH2 P213L-induced myelin abnormalities in the pathogenesis of ID.Mechanistically,the P213L mutation disrupts the interaction between hnRNPH2 and its target transcripts,leading to the downregulation of myelination-related genes.Collectively,these findings reveal a critical mechanistic connection between myelin dysfunction and ID,thereby offering potential therapeutic insights for X-linked neurodevelopmental disorders. 展开更多
关键词 HNRNPH2 RNA binding protein Intellectual disability Myelination Oligodendrocyte differentiation
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Zebrafish optic nerve regeneration involves resident and retinal oligodendrocytes 认领 引用
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作者 Cristina Pérez-Montes Rosalía Hernández-García +5 位作者 Jhoana Paola Jiménez-Cubides Laura DeOliveira-Mello Almudena Velasco Rosario Arévalo Marina García-Macia Adrián Santos-Ledo 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第2期811-820,共10页
The visual system of teleost fish grows continuously,which is a useful model for studying regeneration of the central nervous system.Glial cells are key for this process,but their contribution is still not well define... The visual system of teleost fish grows continuously,which is a useful model for studying regeneration of the central nervous system.Glial cells are key for this process,but their contribution is still not well defined.We followed oligodendrocytes in the visual system of adult zebrafish during regeneration of the optic nerve at 6,24,and 72 hours post-lesion and at 7 and 14 days post-lesion via the sox10:tagRFP transgenic line and confocal microscopy.To understand the changes that these oligodendrocytes undergo during regeneration,we used Sox2 immunohistochemistry,a stem cell marker involved in oligodendrocyte differentiation.We also used the Click-iT™ Plus TUNEL assay to study cell death and a BrdU assay to determine cell proliferation.Before optic nerve crush,sox10:tagRFP oligodendrocytes are located in the retina,in the optic nerve head,and through all the entire optic nerve.Sox2-positive cells are present in the peripheral germinal zone,the mature retina,and the optic nerve.After optic nerve crush,sox10:tagRFP cells disappeared from the optic nerve crush zone,suggesting that they died,although they were not TUNEL positive.Concomitantly,the number of Sox2-positive cells increased around the crushed area,the optic nerve head,and the retina.Then,between 24 hours post-lesion and 14 days post-lesion,double sox10:tagRFP/Sox2-positive cells were detected in the retina,optic nerve head,and whole optic nerve,together with a proliferation response at 72 hours post-lesion.Our results confirm that a degenerating process may occur prior to regeneration.First,sox10:tagRFP oligodendrocytes that surround the degenerated axons stop wrapping them,change their“myelinating oligodendrocyte”morphology to a“nonmyelinating oligodendrocyte”morphology,and die.Then,residual oligodendrocyte progenitor cells in the optic nerve and retina proliferate and differentiate for the purpose of remyelination.As new axons arise from the surviving retinal ganglion cells,new sox10:tagRFP oligodendrocytes arise from residual oligodendrocyte progenitor cells to guide,nourish and myelinate them.Thus,oligodendrocytes play an active role in zebrafish axon regeneration and remyelination. 展开更多
关键词 cell death oligodendrocytes optic nerve proliferation regeneration Sox10 Sox2 visual system zebrafish
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Oligodendrocyte ferroptosis:Novel mechanisms in multiple sclerosis 认领 引用
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作者 Valentina Saverio Dmitry Lim Marco Corazzari 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第8期3561-3562,共2页
Myelination in the central nervous system(CNS)is a highly intricate process,exclusive to vertebrates,that relies on the coordinated interaction between oligodendrocytes(OLs)and neurons.In addition to their role in for... Myelination in the central nervous system(CNS)is a highly intricate process,exclusive to vertebrates,that relies on the coordinated interaction between oligodendrocytes(OLs)and neurons.In addition to their role in forming myelin,accumulating evidence indicates that OLs provide crucial trophic support to axons,contributing to normal CNS function.Notably,OL injury and loss are observed in a variety of human conditions,including stroke,traumatic injuries of the brain and spinal cord,as well as neurodegenerative disorders such as multiple sclerosis(MS). 展开更多
关键词 central nervous system central nervous system cns ferroptosis oligodendrocyte myelination multiple sclerosis vertebrates trophic support
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Autophagy in Oligodendrocyte Lineage Cells Controls Oligodendrocyte Numbers and Myelin Integrity in an Age‑dependent Manner 认领 引用 被引量：2
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作者 Hong Chen Gang Yang +8 位作者 De‑En Xu Yu‑tong Du Chao Zhu Hua Hu Li Luo Lei Feng Wenhui Huang Yan‑Yun Sun Quan‑Hong Ma 《Neuroscience Bulletin》 SCIE CAS CSCD 2025年第3期374-390,共17页
Oligodendrocyte lineage cells, including oligodendrocyte precursor cells (OPCs) and oligodendrocytes (OLs), are essential in establishing and maintaining brain circuits. Autophagy is a conserved process that keeps the... Oligodendrocyte lineage cells, including oligodendrocyte precursor cells (OPCs) and oligodendrocytes (OLs), are essential in establishing and maintaining brain circuits. Autophagy is a conserved process that keeps the quality of organelles and proteostasis. The role of autophagy in oligodendrocyte lineage cells remains unclear. The present study shows that autophagy is required to maintain the number of OPCs/OLs and myelin integrity during brain aging. Inactivation of autophagy in oligodendrocyte lineage cells increases the number of OPCs/OLs in the developing brain while exaggerating the loss of OPCs/OLs with brain aging. Inactivation of autophagy in oligodendrocyte lineage cells impairs the turnover of myelin basic protein (MBP). It causes MBP to accumulate in the cytoplasm as multimeric aggregates and fails to be incorporated into integral myelin, which is associated with attenuated endocytic recycling. Inactivation of autophagy in oligodendrocyte lineage cells impairs myelin integrity and causes demyelination. Thus, this study shows autophagy is required to maintain myelin quality during aging by controlling the turnover of myelin components. 展开更多
关键词 Autophagy Oligodendrocyte precursor cells Oligodendrocytes Myelination Myelin proteins Turnover Degradation
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Perilipin-2 mediates ferroptosis in oligodendrocyte progenitor cells and myelin injury after ischemic stroke 认领 引用 被引量：9
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作者 Jian Yang Jiang Wu +7 位作者 Xueshun Xie Pengfei Xia Jinxin Lu Jiale Liu Lei Bai Xiang Li Zhengquan Yu Haiying Li 《Neural Regeneration Research》 SCIE CAS CSCD 2025年第7期2015-2028,共14页
Differentiation of oligodendrocyte progenitor cells into mature myelin-forming oligodendrocytes contributes to remyelination.Failure of remyelination due to oligodendrocyte progenitor cell death can result in severe n... Differentiation of oligodendrocyte progenitor cells into mature myelin-forming oligodendrocytes contributes to remyelination.Failure of remyelination due to oligodendrocyte progenitor cell death can result in severe nerve damage.Ferroptosis is an iron-dependent form of regulated cell death caused by membrane rupture induced by lipid peroxidation,and plays an important role in the pathological process of ischemic stroke.However,there are few studies on oligodendrocyte progenitor cell ferroptosis.We analyzed transcriptome sequencing data from GEO databases and identified a role of ferroptosis in oligodendrocyte progenitor cell death and myelin injury after cerebral ischemia.Bioinformatics analysis suggested that perilipin-2(PLIN2)was involved in oligodendrocyte progenitor cell ferroptosis.PLIN2 is a lipid storage protein and a marker of hypoxia-sensitive lipid droplet accumulation.For further investigation,we established a mouse model of cerebral ischemiaeperfusion.We found significant myelin damage after cerebral ischemia,as well as oligodendrocyte progenitor cell death and increased lipid peroxidation levels around the infarct area.The ferroptosis inhibitor,ferrostatin-1,rescued oligodendrocyte progenitor cell death and subsequent myelin injury.We also found increased PLIN2 levels in the peri-infarct area that co-localized with oligodendrocyte progenitor cells.Plin2 knockdown rescued demyelination and improved neurological deficits.Our findings suggest that targeting PLIN2 to regulate oligodendrocyte progenitor cell ferroptosis may be a potential therapeutic strategy for rescuing myelin damage after cerebral ischemia. 展开更多
关键词 bioinformatics bulk RNA sequencing ferroptosis ischemic stroke myelin injury oligodendrocyte progenitor cell perilipin-2 single-cell RNA sequencing
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13-Docosenamide Enhances Oligodendrocyte Precursor Cell Differentiation via USP33-Mediated Deubiquitination of CNR1 in Chronic Cerebral Hypoperfusion 认领 引用
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作者 Yuhao Xu Yi Tan +7 位作者 Zhi Zhang Duo Chen Chao Zhou Liang Sun Shengnan Xia Xinyu Bao Haiyan Yang Yun Xu 《Neuroscience Bulletin》 SCIE CAS CSCD 2025年第11期1939-1956,共18页
Chronic cerebral hypoperfusion leads to white matter injury(WMI),which plays a significant role in contributing to vascular cognitive impairment.While 13-docosenamide is a type of fatty acid amide,it remains unclear w... Chronic cerebral hypoperfusion leads to white matter injury(WMI),which plays a significant role in contributing to vascular cognitive impairment.While 13-docosenamide is a type of fatty acid amide,it remains unclear whether it has therapeutic effects on chronic cerebral hypoperfusion.In this study,we conducted bilateral common carotid artery stenosis(BCAS)surgery to simulate chronic cerebral hypoperfusion-induced WMI and cognitive impairment.Our findings showed that 13-docosenamide alleviates WMI and cognitive impairment in BCAS mice.Mechanistically,13-docosenamide specifically binds to cannabinoid receptor 1(CNR1)in oligodendrocyte precursor cells(OPCs).This interaction results in an upregulation of ubiquitin-specific peptidase 33(USP33)-mediated CNR1 deubiquitination,subsequently increasing CNR1 protein expression,activating the phosphorylation of the AKT/mTOR pathway,and promoting the differentiation of OPCs.In conclusion,our study suggests that 13-docosenamide can ameliorate chronic cerebral hypoperfusion-induced WMI and cognitive impairment by enhancing OPC differentiation and could serve as a potential therapeutic drug. 展开更多
关键词 13-Docosenamide White matter injury Oligodendrocyte precursor cell Cannabinoid receptor 1 Ubiquitin-specifc peptidase 33
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Oligodendrocyte Precursor Cell-Specific HMGB1 Knockout Reduces Immune Cell Infiltration and Demyelination in Experimental Autoimmune Encephalomyelitis Models 认领 引用 被引量：1
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作者 Gyuree Kim JiHye Seo +4 位作者 Bokyung Kim Young-Ho Park Hong Jun Lee Fuzheng Guo Dong-Seok Lee 《Neuroscience Bulletin》 SCIE CAS CSCD 2025年第7期1145-1160,共16页
Infiltration and activation of peripheral immune cells are critical in the progression of multiple sclerosis and its experimental animal model,experimental autoimmune encephalomyelitis(EAE).This study investigates the... Infiltration and activation of peripheral immune cells are critical in the progression of multiple sclerosis and its experimental animal model,experimental autoimmune encephalomyelitis(EAE).This study investigates the role of high mobility group box 1(HMGB1)in oligodendrocyte precursor cells(OPCs)in modulating pathogenic T cells infiltrating the central nervous system through the blood-brain barrier(BBB)by using OPC-specific HMGB1 knockout(KO)mice.We found that HMGB1 released from OPCs promotes BBB disruption,subsequently allowing increased immune cell infiltration.The migration of CD4+T cells isolated from EAE-induced mice was enhanced when co-cultured with OPCs compared to oligodendrocytes(OLs).OPC-specific HMGB1 KO mice exhibited lower BBB permeability and reduced immune cell infiltration into the CNS,leading to less damage to the myelin sheath and mitigated EAE progression.CD4+T cell migration was also reduced when co-cultured with HMGB1 knock-out OPCs.Our findings reveal that HMGB1 secretion from OPCs is crucial for regulating immune cell infiltration and provides insights into the immunomodulatory function of OPCs in autoimmune diseases. 展开更多
关键词 Multiple sclerosis High mobility group box 1 Oligodendrocyte precursor cell Experimental autoimmune encephalomyelitis
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Cation Channel TMEM63A Autonomously Facilitates Oligodendrocyte Differentiation at an Early Stage 认领 引用
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作者 Yue-Ying Wang Dan Wu +12 位作者 Yongkun Zhan Fei Li Yan-Yu Zang Xiao-Yu Teng Linlin Zhang Gui-Fang Duan He Wang Rong Xu Guiquan Chen Yun Xu Jian-Jun Yang Yongguo Yu Yun Stone Shi 《Neuroscience Bulletin》 SCIE CAS CSCD 2025年第4期615-632,共18页
Accurate timing of myelination is crucial for the proper functioning of the central nervous system. Here, we identified a de novo heterozygous mutation in TMEM63A (c.1894G>A;p. Ala632Thr) in a 7-year-old boy exhibi... Accurate timing of myelination is crucial for the proper functioning of the central nervous system. Here, we identified a de novo heterozygous mutation in TMEM63A (c.1894G>A;p. Ala632Thr) in a 7-year-old boy exhibiting hypomyelination. A Ca2+ influx assay suggested that this is a loss-of-function mutation. To explore how TMEM63A deficiency causes hypomyelination, we generated Tmem63a knockout mice. Genetic deletion of TMEM63A resulted in hypomyelination at postnatal day 14 (P14) arising from impaired differentiation of oligodendrocyte precursor cells (OPCs). Notably, the myelin dysplasia was transient, returning to normal levels by P28. Primary cultures of Tmem63a−/− OPCs presented delayed differentiation. Lentivirus-based expression of TMEM63A but not TMEM63A_A632T rescued the differentiation of Tmem63a−/− OPCs in vitro and myelination in Tmem63a−/− mice. These data thus support the conclusion that the mutation in TMEM63A is the pathogenesis of the hypomyelination in the patient. Our study further demonstrated that TMEM63A-mediated Ca2+ influx plays critical roles in the early development of myelin and oligodendrocyte differentiation. 展开更多
关键词 TMEM63A Mutation Oligodendrocyte differentiation Hypomyelination
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Catalpol Promotes Differentiation of Neural Stem Cells into Oligodendrocyte via Caveolin-1-dependent Pathway in The 3D Microfluidic Chip 认领 引用
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作者 WANG Ya-Chen WANG Liang +1 位作者 SHEN Li-Ming LIU Jing 《生物化学与生物物理进展》 SCIE CAS CSCD 北大核心 2025年第11期2842-2853,共12页
Objective Cerebral palsy(CP)is a prevalent neurodevelopmental disorder acquired during the perinatal period,with periventricular white matter injury(PWMI)serving as its primary pathological hallmark.PWMI is characteri... Objective Cerebral palsy(CP)is a prevalent neurodevelopmental disorder acquired during the perinatal period,with periventricular white matter injury(PWMI)serving as its primary pathological hallmark.PWMI is characterized by the loss of oligodendrocytes(OLs)and the disintegration of myelin sheaths,leading to impaired neural connectivity and motor dysfunction.Neural stem cells(NSCs)represent a promising regenerative source for replenishing lost OLs;however,conventional twodimensional(2D)in vitro culture systems lack the three-dimensional(3D)physiological microenvironment.Microfluidic chip technology has emerged as a powerful tool to overcome this limitation by enabling precise spatial and temporal control over 3D microenvironmental conditions,including the establishment of stable concentration gradients of bioactive molecules.Catalpol,an iridoid glycoside derived from traditional medicinal plants,exhibits dual antioxidant and anti-apoptotic properties.Despite its therapeutic potential,the capacity of catalpol to drive NSC differentiation toward OLs under biomimetic 3D conditions,as well as the underlying molecular mechanisms,remains poorly understood.This study aims to develop a microfluidic-based 3D biomimetic platform to systematically investigate the concentration-dependent effects of catalpol on promoting NSCs-to-OLs differentiation and to elucidate the role of the caveolin-1(Cav-1)signaling pathway in this process.Methods We developed a novel multiplexed microfluidic device featuring parallel microchannels with integrated gradient generators capable of establishing and maintaining precise linear concentration gradients(0-3 g/L catalpol)across 3D NSCs cultures.This platform facilitated the continuous perfusion culture of NSC-derived 3D spheroids,mimicking the dynamic in vivo microenvironment.Real-time cell viability was assessed using Calcein-AM/propidium iodide(PI)dual staining,with fluorescence imaging quantifying live/dead cell ratios.Oligodendrocyte differentiation was evaluated through quantitative reverse transcription polymerase chain reaction(qRT-PCR)for MBP and SOX10 gene expression,complemented by immunofluorescence staining to visualize corresponding protein changes.To dissect the molecular mechanism,the Cav-1-specific pharmacological inhibitor methyl‑β‑cyclodextrin(MCD)was employed to perturb the pathway,and its effects on differentiation markers were analyzed.Results Catalpol demonstrated excellent biocompatibility,with cell viability exceeding 96%across the entire tested concentration range(0-3 g/L),confirming its non-cytotoxic nature.At the optimal concentration of 0-3 g/L,catalpol significantly upregulated both MBP and SOX10 expression(P<0.05,P<0.01),indicating robust promotion of oligodendroglial differentiation.Intriguingly,Cav-1 mRNA expression was progressively downregulated during NSC differentiation into OLs.Further inhibition of Cav-1 with MCD further enhanced this effect,leading to a statistically significant increase in OL-specific gene expression(P<0.05,P<0.01),suggesting Cav-1 acts as a negative regulator of OLs differentiation.Conclusion This study established an integrated microfluidic gradient chip-3D NSC spheroid culture system,which combines the advantages of precise chemical gradient control with physiologically relevant 3D cell culture.The findings demonstrate that 3 g/L catalpol effectively suppresses Cav-1 signaling to drive NSC differentiation into functional OLs.This work not only provides novel insights into the Cav-1-dependent mechanisms of myelination but also delivers a scalable technological platform for future research on remyelination therapies,with potential applications in cerebral palsy and other white matter disorders.The platform’s modular design permits adaptation for screening other neurogenic compounds or investigating additional signaling pathways involved in OLs maturation. 展开更多
关键词 catalpol neural stem cells oligodendrocytes differentiation caveolin-1 microfluidic chip
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Oligodendrocytes in central nervous system diseases:the effect of cytokine regulation 认领 引用 被引量：8
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作者 Chengfu Zhang Mengsheng Qiu Hui Fu 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第10期2132-2143,共12页
Cytokines including tumor necrosis factor, interleukins, interferons, and chemokines are abundantly produced in various diseases. As pleiotropic factors, cytokines are involved in nearly every aspect of cellular funct... Cytokines including tumor necrosis factor, interleukins, interferons, and chemokines are abundantly produced in various diseases. As pleiotropic factors, cytokines are involved in nearly every aspect of cellular functions such as migration, survival, proliferation, and differentiation. Oligodendrocytes are the myelin-forming cells in the central nervous system and play critical roles in the conduction of action potentials, supply of metabolic components for axons, and other functions. Emerging evidence suggests that both oligodendrocytes and oligodendrocyte precursor cells are vulnerable to cytokines released under pathological conditions. This review mainly summarizes the effects of cytokines on oligodendrocyte lineage cells in central nervous system diseases. A comprehensive understanding of the effects of cytokines on oligodendrocyte lineage cells contributes to our understanding of central nervous system diseases and offers insights into treatment strategies. 展开更多
关键词 astrocyte central nervous system disease CXC chemokine cytokine interferonγ interleukin microglia oligodendrocyte oligodendrocyte precursor cell tumor necrosis factorα
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New insights into the immunologic role of oligodendrocyte lineage cells in demyelination diseases 认领 引用 被引量：3
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作者 Hui Li Yang Chen +1 位作者 Jianqin Niu Chenju Yi 《Journal of Biomedical Research》 CAS CSCD 2022年第5期343-352,共10页
Oligodendrocyte lineage cells(OL-lineage cells)are a cell population that are crucial for mammalian central nervous system(CNS)myelination.OL-lineage cells go through developmental stages,initially differentiating int... Oligodendrocyte lineage cells(OL-lineage cells)are a cell population that are crucial for mammalian central nervous system(CNS)myelination.OL-lineage cells go through developmental stages,initially differentiating into oligodendrocyte precursor cells(OPCs),before becoming immature oligodendrocytes,then mature oligodendrocytes(OLs).While the main function of cell lineage is in myelin formation,and increasing number of studies have turned to explore the immunological characteristics of these cells.Initially,these studies focused on discovering how OPCs and OLs are affected by the immune system,and then,how these immunological changes influence the myelination process.However,recent studies have uncovered another feature of OL-lineage cells in our immune systems.It would appear that OL-lineage cells also express immunological factors such as cytokines and chemokines in response to immune activation,and the expression of these factors changes under various pathologic conditions.Evidence suggests that OL-lineage cells actually modulate immune functions.Indeed,OL-lineage cells appear to play both"victim"and"agent"in the CNS which raises a number of questions.Here,we summarize immunologic changes in OL-lineage cells and their effects,as well as consider OL-lineage cell changes which influence immune cells under pathological conditions.We also describe some of the underlying mechanisms of these changes and their effects.Finally,we describe several studies which use OL-lineage cells as immunotherapeutic targets for demyelination diseases. 展开更多
关键词 oligodendrocyte oligodendrocyte precursor cell demyelination disease multiple sclerosis immunology
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Oligodendrocyte pathology in fetal alcohol spectrum disorders 认领 引用 被引量：3
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作者 Nune Darbinian Michael E.Selzer 《Neural Regeneration Research》 SCIE CAS CSCD 2022年第3期497-502,共6页
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 abnor... 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 which fetuses are at risk and to intervene therapeutically early in the pregnancy. 展开更多
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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Expression of hypoxia-inducible factor 1 alpha and oligodendrocyte lineage gene-1 in cultured brain slices after oxygen-glucose deprivation 认领 引用 被引量：1
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作者 Hong Cui Weijuan Han +1 位作者 Lijun Yang Yanzhong Chang 《Neural Regeneration Research》 SCIE CAS CSCD 2013年第4期328-337,共10页
Oligodendrocyte lineage gene-1 expressed in oligodendrocytes may trigger the repair of neuronal myelin impairment, and play a crucial role in myelin repair. Hypoxia-inducible factor la, a transcription factor, is of g... Oligodendrocyte lineage gene-1 expressed in oligodendrocytes may trigger the repair of neuronal myelin impairment, and play a crucial role in myelin repair. Hypoxia-inducible factor la, a transcription factor, is of great significance in premature infants with hypoxic-ischemic brain damage There is little evidence of direct regulatory effects of hypoxia-inducible factor le on oligodendrocyte lineage gene-l. In this study, brain slices of Sprague-Dawley rats were cultured and subjected to oxygen-glucose deprivation. Then, slices were transfected with hypoxia-inducible factor la or oligodendrocyte lineage gene-1. The expression levels of hypoxia-inducible factor la and oligodendrocyte lineage gene-1 were significantly up-regulated in rat brains prior to transfection, as detected by immunohistochemical staining. Eight hours after transfection of slices with hypoxia-inducible factor la, oligodendrocyte lineage gene-1 expression was upregulated, and reached a peak 24 hours after transfection. Oligodendrocyte lineage gene-1 transfection induced no significant differences in hypoxia-inducible factor la levels in rat brain tissues with oxygen-glucose deprivation. These experimental findings indicate that hypoxia-inducible factor la can regulate oligodendrocyte lineage gene-1 expression in hypoxic brain tissue, thus repairing the neural impairment. 展开更多
关键词 neural regeneration brain injury biological factors hypoxia-inducible factor la oligodendrocyte lineage gene-1 oxygen-glucose deprivation brain slice culture immunohistochemistry oligodendrocyte myelin repair premature delivery rat grants-supported paper photographs-containing paper neuroregeneration
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The contribution of oligodendrocytes and oligodendrocyte progenitor cells to central nervous system repair in multiple sclerosis: perspectives for remyelination therapeutic strategies 认领 引用 被引量：11
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作者 Adriana Octaviana Dulamea 《Neural Regeneration Research》 SCIE CAS CSCD 2017年第12期1939-1944,共6页
Oligodencrocytes（OLs） are the main glial cells of the central nervous system involved in myelination of axons. In multiple sclerosis（MS）, there is an imbalance between demyelination and remyelination processes, th... Oligodencrocytes（OLs） are the main glial cells of the central nervous system involved in myelination of axons. In multiple sclerosis（MS）, there is an imbalance between demyelination and remyelination processes, the last one performed by oligodendrocyte progenitor cells（OPCs） and OLs, resulting into a permanent demyelination, axonal damage and neuronal loss. In MS lesions, astrocytes and microglias play an important part in permeabilization of blood-brain barrier and initiation of OPCs proliferation. Migration and differentiation of OPCs are influenced by various factors and the process is finalized by insufficient acummulation of OLs into the MS lesion. In relation to all these processes, the author will discuss the potential targets for remyelination strategies. 展开更多
关键词 multiple sclerosis oligodencrocytes oligodendrocyte progenitor cells demyelination remyelination semaphorin basic helix-loop-helix transcription factor oligodendrocyte transcription factor 2 leucin-rich repeatand immunoglobulin-like-domain-containing nogo receptor-interacting protein I canonical Notch signaling endocrine receptors
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Oligodendrocyte transcription factor 1 overexpression promotes oligodendrocyte transcription factor 2 expression in the brains of neonatal rats exposed to hypoxia 认领 引用 被引量：1
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作者 Lijun Yang Hong Cui +1 位作者 Aijun Yang Wenxing Jiang 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第34期2713-2717,共5页
To examine the expression profiles of oligodendrocyte transcription factors 1 and 2(Oligl and Olig2)and the interaction between these two proteins,Oligl was transfected into the lateral ventricles of neonatal rats sub... To examine the expression profiles of oligodendrocyte transcription factors 1 and 2(Oligl and Olig2)and the interaction between these two proteins,Oligl was transfected into the lateral ventricles of neonatal rats subjected to hypoxia.Immunohistochemistry demonstrated that Olig2 was expressed throughout the nuclei in the brain,and expression increased at 3 days following hypoxia and was higher than levels at 7 days following Ad5-Oligl transfection.Western blot revealed that Oligl and Olig2 expression increased in Oligl-transfected brain cells 3 days after hypoxia,but Oligl and Olig2 expression decreased at 7 days.These results indicate that Oligl overexpression enhances Olig2 expression in brain tissues of hypoxia rats. 展开更多
关键词 oligodendrocyte transcription factor 1 oligodendrocyte transcription factor 2 hypoxia neonatal rat gene transfection neural regeneration
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Oligodendrocyte precursor cell maturation: role of adenosine receptors 认领 引用 被引量：4
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作者 Federica Cherchi Anna Maria Pugliese Elisabetta Coppi 《Neural Regeneration Research》 SCIE CAS CSCD 2021年第9期1686-1692,共7页
Oligodendrocyte-formed myelin sheaths allow fast synaptic transmission in the brain and their degeneration leads to demyelinating diseases such as multiple sclerosis. Remyelination requires the differentiation of olig... Oligodendrocyte-formed myelin sheaths allow fast synaptic transmission in the brain and their degeneration leads to demyelinating diseases such as multiple sclerosis. Remyelination requires the differentiation of oligodendrocyte progenitor cells into mature oligodendrocytes but, in chronic neurodegenerative disorders, remyelination fails due to adverse environment. Therefore, a strategy to prompt oligodendrocyte progenitor cell differentiation towards myelinating oligodendrocytes is required. The neuromodulator adenosine, and its receptors(A1, A(2A), A(2B) and A3 receptors: A1R, A(2A)R, A(2B)R and A3R), are crucial mediators in remyelination processes. It is known that A1Rs facilitate oligodendrocyte progenitor cell maturation and migration whereas the A3Rs initiates apoptosis in oligodendrocyte progenitor cells. Our group of research contributed to the field by demonstrating that A(2A)R and A(2B)R inhibit oligodendrocyte progenitor cell maturation by reducing voltage-dependent K^+ currents necessary for cell differentiation. The present review summarizes the possible role of adenosine receptor ligands as potential therapeutic targets in demyelinating pathologies such as multiple sclerosis. 展开更多
关键词 adenosine receptors K^+channels oligodendrocyte differentiation oligodendrocyte progenitor cells remyelination
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