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Effects of miR-219/miR-338 on microglia and astrocyte behaviors and astrocyte-oligodendrocyte precursor cell interactions 预览
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作者 Lan Huong Nguyen William Ong +3 位作者 Kai Wang Mingfeng Wang Dean Nizetic Sing Yian Chew 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第4期739-747,共9页
MiR-219 and miR-338(miR-219/miR-338)are oligodendrocyte-specific microRNAs.The overexpression of these miRs in oligodendrocyte precursor cells promotes their differentiation and maturation into oligodendrocytes,which ... MiR-219 and miR-338(miR-219/miR-338)are oligodendrocyte-specific microRNAs.The overexpression of these miRs in oligodendrocyte precursor cells promotes their differentiation and maturation into oligodendrocytes,which may enhance axonal remyelination after nerve injuries in the central nervous system(CNS).As such,the delivery of miR-219/miR-338 to the CNS to promote oligodendrocyte precursor cell differentiation,maturation and myelination could be a promising approach for nerve repair.However,nerve injuries in the CNS also involve other cell types,such as microglia and astrocytes.Herein,we investigated the effects of miR-219/miR-338 treatment on microglia and astrocytes in vitro and in vivo.We found that miR-219/miR-338 diminished microglial expression of pro-inflammatory cytokines and suppressed astrocyte activation.In addition,we showed that miR-219/miR-338 enhanced oligodendrocyte precursor cell differentiation and maturation in a scratch assay paradigm that re-created a nerve injury condition in vitro.Collectively,our results suggest miR-219/miR-338 as a promising treatment for axonal remyelination in the CNS following nerve injuries.All experimental procedures were approved by the Institutional Animal Care and Use Committee(IACUC),Nanyang Technological University(approval No.A0309 and A0333)on April 27,2016 and October 8,2016. 展开更多
关键词 central nervous system electrospinning gene SILENCING GLIA hydrogel MYELINATION nanofibers oligodendroglial POLYCAPROLACTONE spinal cord injury
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Trophic factors are essential for the survival of grafted oligodendrocyte progenitors and for neuroprotection after perinatal excitotoxicity 预览
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作者 Megumi Hirose-Ikeda Brian Chu +5 位作者 Paul Zhao Omar Akil Elida Escalante Laurent Vergnes Carlos Cepeda Araceli Espinosa-Jeffrey 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第3期557-568,共12页
The consequences of neonatal white matter injury are devastating and represent a major societal problem as currently there is no cure.Prematurity,low weight birth and maternal pre-natal infection are the most frequent... The consequences of neonatal white matter injury are devastating and represent a major societal problem as currently there is no cure.Prematurity,low weight birth and maternal pre-natal infection are the most frequent causes of acquired myelin deficiency in the human neonate leading to cerebral palsy and cognitive impairment.In the developing brain,oligodendrocyte(OL)maturation occurs perinatally,and immature OLs are particularly vulnerable.Cell replacement therapy is often considered a viable option to replace progenitors that die due to glutamate excitotoxicity.We previously reported directed specification and mobilization of endogenous committed and uncommitted neural progenitors by the combination of transferrin and insulin growth factor 1(TSC1).Here,considering cell replacement and integration as therapeutic goals,we examined if OL progenitors(OLPs)grafted into the brain parenchyma of mice that were subjected to an excitotoxic insult could rescue white matter injury.For that purpose,we used a well-established model of glutamate excitotoxic injury.Four-day-old mice received a single intraparenchymal injection of the glutamate receptor agonist N-methyl-D-aspartate alone or in conjunction with TSC1 in the presence or absence of OLPs grafted into the brain parenchyma.Energetics and expression of stress proteins and OL developmental specific markers were examined.A comparison of the proteomic profile per treatment was also ascertained.We found that OLPs did not survive in the excitotoxic environment when grafted alone.In contrast,when combined with TSC1,survival and integration of grafted OLPs was observed.Further,energy metabolism in OLPs was significantly increased by N-methyl-D-aspartate and modulated by TSC1.The proteomic profile after the various treatments showed elevated ubiquitination and stress/heat shock protein 90 in response to N-methyl-D-aspartate.These changes were reversed in the presence of TSC1 and ubiquitination was decreased.The results obtained in this pre-clinical study indicate that the use 展开更多
关键词 MYELIN regeneration MYELINATION OLIGODENDROCYTES periventricular leukomalacia premature birth proteomics TROPHIC factors white matter injury
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Glutamate receptors and glutamatergic signalling in the peripheral nerves 预览
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作者 Ting-Jiun Chen Maria Kukley 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第3期438-447,共10页
In the peripheral nervous system,the vast majority of axons are accommodated within the fibre bundles that constitute the peripheral nerves.Axons within the nerves are in close contact with myelinating glia,the Schwan... In the peripheral nervous system,the vast majority of axons are accommodated within the fibre bundles that constitute the peripheral nerves.Axons within the nerves are in close contact with myelinating glia,the Schwann cells that are ideally placed to respond to,and possibly shape,axonal activity.The mechanisms of intercellular communication in the peripheral nerves may involve direct contact between the cells,as well as signalling via diffusible substances.Neurotransmitter glutamate has been proposed as a candidate extracellular molecule mediating the cross-talk between cells in the peripheral nerves.Two types of experimental findings support this idea:first,glutamate has been detected in the nerves and can be released upon electrical or chemical stimulation of the nerves;second,axons and Schwann cells in the peripheral nerves express glutamate receptors.Yet,the studies providing direct experimental evidence that intercellular glutamatergic signalling takes place in the peripheral nerves during physiological or pathological conditions are largely missing.Remarkably,in the central nervous system,axons and myelinating glia are involved in glutamatergic signalling.This signalling occurs via different mechanisms,the most intriguing of which is fast synaptic communication between axons and oligodendrocyte precursor cells.Glutamate receptors and/or synaptic axon-glia signalling are involved in regulation of proliferation,migration,and differentiation of oligodendrocyte precursor cells,survival of oligodendrocytes,and re-myelination of axons after damage.Does synaptic signalling exist between axons and Schwann cells in the peripheral nerves?What is the functional role of glutamate receptors in the peripheral nerves?Is activation of glutamate receptors in the nerves beneficial or harmful during diseases?In this review,we summarise the limited information regarding glutamate release and glutamate receptors in the peripheral nerves and speculate about possible mechanisms of glutamatergic signalling in the nerves.We highli 展开更多
关键词 AMPA RECEPTORS axons GLUTAMATE METABOTROPIC GLUTAMATE RECEPTORS MYELINATION nerve injury NMDA RECEPTORS peripheral nervous system PNS Schwann cells synaptic SIGNALLING
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A method to deliver patterned electrical impulses to Schwann cells cultured on an artificial axon 预览
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作者 Antonio Merolli Yong Mao +3 位作者 Gregory Voronin Joseph A.M.Steele N.Sanjeeva Murthy Joachim Kohn 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第6期1052-1059,共8页
Information from the brain travels back and forth along peripheral nerves in the form of electrical impulses generated by neurons and these impulses have repetitive patterns.Schwann cells in peripheral nerves receive ... Information from the brain travels back and forth along peripheral nerves in the form of electrical impulses generated by neurons and these impulses have repetitive patterns.Schwann cells in peripheral nerves receive molecular signals from axons to coordinate the process of myelination.There is evidence,however,that non-molecular signals play an important role in myelination in the form of patterned electrical impulses generated by neuronal activity.The role of patterned electrical impulses has been investigated in the literature using co-cultures of neurons and myelinating cells.The co-culturing method,however,prevents the uncoupling of the direct effect of patterned electrical impulses on myelinating cells from the indirect effect mediated by neurons.To uncouple these effects and focus on the direct response of Schwann cells,we developed an in vitro model where an electroconductive carbon fiber acts as an artificial axon.The fiber provides only the biophysical characteristics of an axon but does not contribute any molecular signaling.In our“suspended wire model”,the carbon fiber is suspended in a liquid media supported by a 3D printed scaffold.Patterned electrical impulses are generated by an Arduino 101 microcontroller.In this study,we describe the technology needed to set-up and eventually replicate this model.We also report on our initial in vitro tests where we were able to document the adherence and ensheath of human Schwann cells to the carbon fiber in the presence of patterned electrical impulses(hSCs were purchased from ScienCell Research Laboratories,Carlsbad,CA,USA;ScienCell fulfills the ethic requirements,including donor’s consent).This technology will likely make feasible to investigate the response of Schwann cells to patterned electrical impulses in the future. 展开更多
关键词 Schwann cell carbon fiber MYELINATION ELECTRICAL impulse artificial AXON in vitro system Arduino microcontroller MYELIN basic protein
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孕期缺铁对婴幼儿运动发育的研究进展
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作者 李明燕(综述) 赵正言(审校) 《中国儿童保健杂志》 CAS 2019年第11期1192-1195,共4页
铁缺乏(ID)和缺铁性贫血(IDA)是全球最常见的单一营养缺乏性疾病。孕妇和婴幼儿是ID的高危人群,孕母ID到一定程度会影响胎儿/新生儿的铁营养状况。早期ID主要通过影响髓鞘化、纹状体和多巴胺神经递质影响个体的运动发育。生后早期给予... 铁缺乏(ID)和缺铁性贫血(IDA)是全球最常见的单一营养缺乏性疾病。孕妇和婴幼儿是ID的高危人群,孕母ID到一定程度会影响胎儿/新生儿的铁营养状况。早期ID主要通过影响髓鞘化、纹状体和多巴胺神经递质影响个体的运动发育。生后早期给予足量的铁剂治疗能纠正婴幼儿循环及组织内的ID,但无法完全逆转孕期ID所致的行为改变。深入研究孕期ID对婴幼儿运动发育的影响及其可逆性,明确铁剂治疗的关键时间窗,对提高儿童生存质量,改善远期预后具有十分重要的意义。 展开更多
关键词 铁缺乏 髓鞘化 多巴胺神经递质 运动发育 婴幼儿
扩散张量成像在新生儿脑髓鞘发育中的初步研究 预览
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作者 郭莉莉 王德杭 +2 位作者 张辉 陶维静 柏根基 《磁共振成像》 CAS 2019年第10期748-751,共4页
目的应用磁共振扩散张量成像(diffusion tensor imaging,DTI)研究新生儿脑白质各向异性分数(fractional anisotropy,FA),探讨DTI在脑白质髓鞘发育中的应用价值.材料与方法收集行常规MRI和DTI扫描足月儿39例(胎龄37~42周)和早产儿61例(... 目的应用磁共振扩散张量成像(diffusion tensor imaging,DTI)研究新生儿脑白质各向异性分数(fractional anisotropy,FA),探讨DTI在脑白质髓鞘发育中的应用价值.材料与方法收集行常规MRI和DTI扫描足月儿39例(胎龄37~42周)和早产儿61例(纠正胎龄至40周),围产史均正常,无神经系统疾病.分别测量各兴趣区的FA值,分析足月儿和早产儿的差异及其在脑内各部位白质的FA值差异.结果①左右半球相同部位的FA值差异无统计学意义(P>0.05).②早产儿和足月儿同部位FA值比较,内囊前后肢、胼胝体压部、半卵圆中心b区及外囊和小脑中脚区FA值两组比较差异有统计学意义(P<0.05).胼胝体膝部、侧脑室前角旁白质、侧脑室后角旁白质、半卵圆中心a区、室管膜下区的FA值两组比较差异无统计学意义(P>0.05).③早产儿和足月儿组内各白质区FA值不同,两两比较均发现内囊后肢高于前肢,侧脑室后角旁白质高于侧脑室前角旁白质,胼胝体压部高于膝部,各差异均有统计学意义(P<0.05).其中侧脑室前角旁白质FA值最低,胼胝体压部和内囊后肢FA值最高,两者比较差异均有统计学意义(P<0.05).结论 DTI的FA值可用于脑髓鞘发育成熟度的定量评价,早产儿和足月儿FA值差异提示早产儿脑内局部区域髓鞘成熟晚.不同区域FA值不同反映髓鞘形成时间的差异. 展开更多
关键词 新生儿 扩散张量成像 髓鞘 磁共振成像
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MYRF与中枢神经系统髓鞘发育 预览
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作者 杜君卿 黄浩 杨爱芬 《杭州师范大学学报:自然科学版》 CAS 2019年第3期249-254,299共7页
在脊椎动物的中枢神经系统中,少突胶质细胞围绕神经元轴突形成髓鞘,使神经冲动可以沿轴突跳跃式快速传导.髓鞘的异常会导致多种神经系统疾病甚至引起死亡.MYRF作为一种转录因子,是目前已知的OLs分化和髓鞘维持的最关键调控因子之一,对M... 在脊椎动物的中枢神经系统中,少突胶质细胞围绕神经元轴突形成髓鞘,使神经冲动可以沿轴突跳跃式快速传导.髓鞘的异常会导致多种神经系统疾病甚至引起死亡.MYRF作为一种转录因子,是目前已知的OLs分化和髓鞘维持的最关键调控因子之一,对MYRF的研究将是髓鞘发育和再生机制的重要内容.文章就近年来MYRF调控中枢神经系统髓鞘发育的研究进展进行了总结. 展开更多
关键词 MYRF 少突胶质细胞 髓鞘形成 髓鞘再生 转录因子
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Olfactory ensheathing cells promote nerve regeneration and functional recovery after facial nerve defects 预览
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作者 Jian Gu He Xu +6 位作者 Ya-Ping Xu Huan-Hai Liu Jun-Tian Lang Xiao-Ping Chen Wei-Hua Xu Yue Deng Jing-Ping Fan 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第1期124-131,共8页
关键词 神经纤维 嗅觉 面部 SPRAGUE-DAWLEY 房间 新生 纤维形态学 厚度测量
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Progesterone effects on the oligodendrocyte linage: all roads lead to the progesterone receptor 预览
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作者 Ignacio Jure Alejandro F. De Nicola Florencia Labombarda 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第12期2029-2034,共6页
A new role has emerged for progesterone after discovering its potent actions away from reproduction in both the central and the peripheral nervous system. The aim of the present report is to discuss progesterone’s me... A new role has emerged for progesterone after discovering its potent actions away from reproduction in both the central and the peripheral nervous system. The aim of the present report is to discuss progesterone’s mechanisms of action involved in myelination, remyelination and neuroinflammation. The pivotal role of the classic progesterone receptor is described and evidence is compiled about progesterone’s direct effects on oligodendrocyte linage and its indirect effects on oligodendrocyte precursor cell differentiation by decreasing the neuroinflammatory environment. 展开更多
关键词 PROGESTERONE PROGESTERONE receptor OLIGODENDROCYTE differentiation MYELINATION REMYELINATION NEUROINFLAMMATION
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Cyclin-dependent Kinase 18 Promotes Oligodendrocyte Precursor Cell Differentiation through Activating the Extracellular Signal-Regulated Kinase Signaling Pathway
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作者 Yuchen Pan Zeping Jiang +6 位作者 Dingya Sun Zhenghao Li Yingyan Pu Dan Wang Aijun Huang Cheng He Li Cao 《神经科学通报:英文版》 SCIE CAS CSCD 2019年第5期802-814,共13页
The correct differentiation of oligodendrocyte precursor cells(OPCs) is essential for the myelination and remyelination processes in the central nervous system.Determining the regulatory mechanism is fundamental to th... The correct differentiation of oligodendrocyte precursor cells(OPCs) is essential for the myelination and remyelination processes in the central nervous system.Determining the regulatory mechanism is fundamental to the treatment of demyelinating diseases. By analyzing the RNA sequencing data of different neural cells, we found that cyclin-dependent kinase 18(CDK18) is exclusively expressed in oligodendrocytes. In vivo studies showed that the expression level of CDK18 gradually increased along with myelin formation during development and in the remyelination phase in a lysophosphatidylcholine-induced demyelination model, and was distinctively highly expressed in oligodendrocytes. In vitro overexpression and interference experiments revealed that CDK18 directly promotes the differentiation of OPCs, without affecting their proliferation or apoptosis. Mechanistically, CDK18 activated the RAS/mitogen-activated protein kinase kinase1/extracellular signal-regulated kinase pathway, thus promoting OPC differentiation. The results of the present study suggest that CDK18 is a promising cell-type specific target to treat demyelinating disease. 展开更多
关键词 OPC OLIGODENDROCYTE MYELINATION CDK18 ERK
芬戈莫德在脑白质缺血损伤中的神经保护研究 预览
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作者 秦川 樊文慧 +1 位作者 刘倩 张强 《中风与神经疾病杂志》 2018年第8期686-689,共4页
目的以临床常见的缺血性脑白质损伤为研究切入点,研究S1P受体激动剂芬戈莫德(FTY720)在小鼠低灌注脑白质损伤后对髓鞘脱失、认知功能障碍的影响,并探讨在小鼠低灌注脑白质损伤后FTY720对小胶质细胞活化、吞噬的影响,FTY720对少突胶质细... 目的以临床常见的缺血性脑白质损伤为研究切入点,研究S1P受体激动剂芬戈莫德(FTY720)在小鼠低灌注脑白质损伤后对髓鞘脱失、认知功能障碍的影响,并探讨在小鼠低灌注脑白质损伤后FTY720对小胶质细胞活化、吞噬的影响,FTY720对少突胶质细胞存活、增殖、分化的影响。方法建立小鼠双侧颈总动脉狭窄(BCAS)模型,通过8臂迷宫行为学测试方法探究FTY720对小鼠造模后认知功能的影响;LFB染色观察FTY720对小鼠造模后髓鞘的影响;共聚焦显微镜观察FTY720干预后小胶质细胞在小鼠低灌注损伤后一个月的变化。结果成功建立小鼠低灌注白质损伤模型(BCAS)。FTY720干预后,白质区域损伤情况明显好于空白对照组。FTY720在低灌注后抑制小胶质细胞活化、吞噬,减轻小鼠的认知功能损害。结论慢性低灌注可以造成选择性的脑白质损伤以及认知功能障碍;FTY720在低灌注后抑制小胶质细胞活化、吞噬,减少髓鞘脱失,改善缺血性脑白质损伤,减轻小鼠的认知功能损害。因此FTY720有望成为缺血性脑白质损伤治疗的潜在靶点。 展开更多
关键词 FTY720 低灌注性脑白质损伤 小胶质细胞 髓鞘脱失
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S5B-2 Maternal Separation and Chronic Social Defeat Impair Prefrontal Cortical Myelination and Cognitive Functions in Rats 预览
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作者 李葆明 《神经药理学报》 2018年第4期83-84,共2页
Adverse life experience induces permanent phenotypic changes in cognitive functions associated with the prefrontal cortex(PFC).However,the underlying mechanisms remain unclear.In this work,we use neonatal maternal sep... Adverse life experience induces permanent phenotypic changes in cognitive functions associated with the prefrontal cortex(PFC).However,the underlying mechanisms remain unclear.In this work,we use neonatal maternal separation(NMS)and chronic social defeat(CSD)rat models to address how adverse life experience affects PFC-dependent cognitive functions.Our results show that normal myelination of the medial PFC(mPFC)is necessary for mPFC-dependent behaviors,as experimental blockade of oligodendrocyte differentiation or lysolecithin-induced demyelination impairs mPFC-dependent behaviors.NMS or CSD produces severe deficits in mPFC myelination,while other brain regions,such as the hippocampusa and basal ganglia,remain intact.In parallel,rats with NMS or CSD exhibit anxiety-like behaviors and demonstrate poor performance on mPFC-dependent tasks.Further experiments demonstrate that,histone deacetylases 1/2(HDAC1/2)are reduced in the mPFC of NMS and CSD rats.Inhibition of HDAC1/2 promotes activation of Wnt signalling,which negatively regulates oligodendrocyte development.Conversely,selective inhibition of Wnt signaling rescues the myelination arrestment and behavioral deficiency induced by NMS or CSD.These findings indicate that NMS or CSD impairs mPFC cognitive functions via regulation of oligodendrogenesis and myelination. 展开更多
关键词 ADVERSE life experience MYELINATION Cognitive functions PREFRONTAL CORTEX Rat
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未成熟大鼠脑白质损伤对miR-219变化的影响
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作者 孙轶 曾进 +6 位作者 李锦潮 陈晓丹 曾菁 方琪 孟兴补 梁淑敏 杨玉莲 《广州医科大学学报》 2018年第4期1-6,共6页
目的:研究miR-219在未成熟大鼠脑白质损伤时的变化,探索早产儿脑白质损伤后髓鞘化障碍的发病机制。方法:缺血缺氧(HI)法建立未成熟大鼠脑白质损伤的动物模型。4日龄SD大鼠随机分为实验组(n=80)和对照组(n=60)。实验组予右侧颈总动脉永... 目的:研究miR-219在未成熟大鼠脑白质损伤时的变化,探索早产儿脑白质损伤后髓鞘化障碍的发病机制。方法:缺血缺氧(HI)法建立未成熟大鼠脑白质损伤的动物模型。4日龄SD大鼠随机分为实验组(n=80)和对照组(n=60)。实验组予右侧颈总动脉永久性结扎后,6%氧气、94%氮气吸入90 min。q PCR检测HI后1 d、3 d、7 d时两组胼胝体miR-219的动态表达变化,免疫印迹检测HI后3 d、7 d时PDGFRα在胼胝体中的表达,Morris水迷宫评估大鼠认知和记忆能力。结果:成功建立了未成熟大鼠脑白质损伤的动物模型,HI后7天两组大鼠胼胝体miR-219的相对表达量均较1天和3天时明显上升(P<0.01),但实验组7 d时miR-219表达量显著低于对照组(6.63±1.39 vs 13.19±2.23,P<0.01);HI后7 d时两组大鼠胼胝体PDGFRα蛋白表达比3天时均有所降低,但实验组7 d时PDGFRα蛋白表达降低较慢,其相对灰度值显著高于对照组(0.93±0.04 vs 0.76±0.05,P<0.01);实验组大鼠HI后14天髓鞘碱性蛋白表达降低,成年期Morris水迷宫实验显示其逃避潜伏期时间长于对照组(P<0.05),第5天60 s内穿越平台次数少于对照组(P<0.05),在目标象限停留的时间百分比低于对照组(P<0.01)。结论:未成熟大鼠脑白质损伤时miR-219的表达在发育过程中其上升趋势受到抑制,并伴有PDGFRα的表达相对增加,提示miR-219在早产儿脑白质损伤后髓鞘化障碍发生机制中发挥重要作用。 展开更多
关键词 miR-219 脑白质损伤 PDGFRΑ 髓鞘化
NG2胶质细胞增殖和分化的研究进展 预览
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作者 刘远 叶云 +2 位作者 李明超 张祚 周吉银 《中国实用神经疾病杂志》 2018年第21期2424-2430,共7页
NG2胶质细胞是哺乳动物中枢神经系统中增生最多的胶质细胞之一,其在发育过程中和成年都具有自我更新或产生新的少突胶质细胞的能力。中枢神经系统损伤后,NG2胶质细胞的增殖能力迅速增加且其分化潜能也变宽,可分化为星形胶质细胞甚至神... NG2胶质细胞是哺乳动物中枢神经系统中增生最多的胶质细胞之一,其在发育过程中和成年都具有自我更新或产生新的少突胶质细胞的能力。中枢神经系统损伤后,NG2胶质细胞的增殖能力迅速增加且其分化潜能也变宽,可分化为星形胶质细胞甚至神经元。但影响其增殖和分化的机制还不明确,故本文对影响NG2胶质细胞的各种信号分子、生长因子及其分化潜能进行综述,进而更好地调控NG2胶质细胞的增殖和分化,更好地发挥其在中枢神经系统病变中的作用。 展开更多
关键词 NG2胶质细胞 增殖 分化 中枢神经系统损伤 分化潜能
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GSK3β inhibitor promotes myelination and mitigates muscle atrophy after peripheral nerve injury 预览
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作者 Jian Weng Yan-hua Wang +2 位作者 Ming Li Dian-ying Zhang Bao-guo Jiang 《中国神经再生研究:英文版》 SCIE CAS CSCD 2018年第2期324-330,共7页
关键词 肌肉萎缩 神经分布 损害 聚合酶链反应 WNT 肌肉细胞 模型设计 调查结果
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CXCL12/CXCR4介导少突胶质前体细胞髓鞘化的作用及调控机制 被引量:2
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作者 余淼 蒋涛 +3 位作者 阴洪 田永阳 李邦银 任先军 《中国矫形外科杂志》 CSCD 北大核心 2017年第10期926-931,共6页
[目的]体外条件下研究CXCL12/CXCR4介导大鼠少突胶质前体细胞(oligodendrocyte precursor cells,OPCs)髓鞘化的作用及影响。[方法]振荡分离、差速贴壁和免疫细胞化学技术分离、培养、鉴定OPCs;Western blotting检测在不同浓度CXCL12(... [目的]体外条件下研究CXCL12/CXCR4介导大鼠少突胶质前体细胞(oligodendrocyte precursor cells,OPCs)髓鞘化的作用及影响。[方法]振荡分离、差速贴壁和免疫细胞化学技术分离、培养、鉴定OPCs;Western blotting检测在不同浓度CXCL12(0、5、10、20 ng/ml)作用下,OPCs髓磷脂碱性蛋白(MBP)和髓鞘脂蛋白(PLP)的表达;CXCR4si RNA干扰CXCR4蛋白表达、LY294002抑制AKT通路活性、U0126抑制ERK通路活性,利用Western blotting检测在20ng/ml CXCL12作用下OPCs髓鞘形成相关蛋白MBP和PLP的表达,并用免疫荧光标记MBP和PLP。[结果]随着细胞外CXCL12的浓度升高,CXCL12能够明显促进OPCs髓鞘形成相关蛋白MBP和PLP的表达。与0 ng/ml相比,CXCL12在20 ng/ml作用后,OPCs髓鞘形成相关蛋白MBP和PLP蛋白表达增加最明显(P〈0.05);干扰CXCR4蛋白表达,抑制AKT、ERK通路活性,OPCs髓鞘形成相关蛋白MBP和PLP蛋白表达受到抑制(P〈0.05)。[结论]体外条件CXCL12/CXCR4对大鼠少突胶质前体细胞参与轴突髓鞘化有促进作用,并且能够通过ERK和PI3K/AKT信号通路对髓鞘形成相关蛋白MBP和PLP蛋白表达进行调控。 展开更多
关键词 少突胶质前体细胞 CXCL12 CXCR4 MBP PLP 髓鞘化
Acta Biomat:开发出可促进机体神经组织再生的新型网格纤维结构
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作者 Koji Suzuki Hiroyuki Tanaka +6 位作者 Mitsuhiro Ebara Koichiro Uto Hozo Matsuoka Shunsuke Nishimoto Kiyoshi Okada Tsuyoshi Murase Hideki Yoshikawa 《现代生物医学进展》 CAS 2017年第18期I0002-I0003,共2页
近日。一项刊登在国际杂志Acta Biomaterialia上的研究报告中。来自日本大阪大学的研究人员通过研究开发出了一种网格结构。其能够被缠绕在损伤的周围神经组织上来帮助促进损伤神经的再生并且恢复其功能。
关键词 损伤神经 组织再生 网格结构 研究开发 纤维结构 机体 日本大阪大学 研究人员
Schwann细胞在髓鞘形成过程中的极性调控 预览
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作者 万丽丹 刘厚奇 丁文龙 《中国组织化学与细胞化学杂志》 CAS CSCD 2017年第4期383-388,共6页
周围神经系统髓鞘形成依赖Schwann细胞和神经元之间复杂的相互作用。细胞极性分子蛋白Par-3在Schwann细胞与轴突接触面密集分布,为BDNF/p75NTR介导的启动成髓提供分子支架。然而,Par-3在该界面聚集并呈不对称性分布的机制仍是一个谜... 周围神经系统髓鞘形成依赖Schwann细胞和神经元之间复杂的相互作用。细胞极性分子蛋白Par-3在Schwann细胞与轴突接触面密集分布,为BDNF/p75NTR介导的启动成髓提供分子支架。然而,Par-3在该界面聚集并呈不对称性分布的机制仍是一个谜。不少研究发现,JAM和nectin等细胞粘附分子与Par-3不对称性分布有关。另外,通过改变轴突信号如神经营养因子和神经素的水平,也能影响Schwann髓鞘的形成。本文综述和阐释在髓鞘形成过程中,Schwann细胞极性是如何被调控的。 展开更多
关键词 SCHWANN细胞 髓鞘形成 细胞极性 Par-3
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过表达Olig2的少突胶质前体细胞在缺血缺氧脑白质损伤新生大鼠脑内的分化
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作者 王晓舟 张振中 +2 位作者 余浩 王宇 姚瑞芹 《神经解剖学杂志》 CSCD 北大核心 2017年第6期685-690,共6页
目的:观察过表达特异性转录因子Ol啦的少突胶质前体细胞(oligodendrocyteprecursorceHs,OPCs)移植在缺血缺氧(hypoxia-ischemia,HI)脑自质损伤新生大鼠脑内的分化情况。方法:用绿色荧光蛋白(greenfluorescentprotein,GFP)标... 目的:观察过表达特异性转录因子Ol啦的少突胶质前体细胞(oligodendrocyteprecursorceHs,OPCs)移植在缺血缺氧(hypoxia-ischemia,HI)脑自质损伤新生大鼠脑内的分化情况。方法:用绿色荧光蛋白(greenfluorescentprotein,GFP)标记的过表达Olig2的慢病毒感染原代分离纯化的大鼠大脑皮层OPCs,GFP阳性细胞计数测其感染率。将过表达0l啦的OPCs(Olig2组)或阴性对照病毒感染的OPCs(Vector组)脑立体定位注射到造模后7d的HI模型大鼠胼胝体膝部,移植后2周,冰冻切片行免疫荧光染色观察OPCs的存活和分化情况。结果:Olig2-GV218病毒感染OPCs细胞48h,荧光显微镜检测显示85%左右的OPCs细胞表达GFP;移植后2周,caspase-3荧光染色表明移植后绝大部分细胞存活,Vector组和0lig2组之间无统计学差异(P〉0.05);GFAP/GFP双阳性细胞在两组之间也无显著差异(P〉0.05);而Olig2组MBP/GFP双阳性细胞的荧光密度显著高于Vector组(P〈0.05)。结论:过表达Oligs2可促进移植OPCs向少突胶质细胞分化。 展开更多
关键词 缺血缺氧 脑白质损伤 细胞移植 OLIG2 髓鞘形成 大鼠
Role of tumor necrosis factor-alpha in zebrafish retinal neurogenesis and myelination
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作者 Xu-Dan Lei Yan Sun +3 位作者 Shi-Jiao Cai Yang-Wu Fang Jian-Lin Cui Yu-Hao Li 《国际眼科杂志:英文版》 SCIE CAS 2016年第6期831-837,共7页
AIM: To investigate the role of tumor necrosis factoralpha(TNF-α) in zebrafish retinal development and myelination.METHODS: Morpholino oligonucleotides(MO), which are complementary to the translation start site of th... AIM: To investigate the role of tumor necrosis factoralpha(TNF-α) in zebrafish retinal development and myelination.METHODS: Morpholino oligonucleotides(MO), which are complementary to the translation start site of the wild-type embryonic zebrafish TNF-α m RNA sequence,were synthesized and injected into one- to four-cell embryos. The translation blocking specificity was verified by Western blotting using an anti-TNF-α antibody,whole-mount in situ hybridization using a hepatocyte-specific m RNA probe ceruloplasmin(cp), and co-injection of TNF-α MO and TNF-α m RNA. An atonal homolog 7(atoh7) m RNA probe was used to detect neurogenesis onset. The retinal neurodifferentiation was analyzed by immunohistochemistry using antibodies Zn12, Zpr1, and Zpr3 to label ganglion cells, cones, and rods, respectively. Myelin basic protein(mbp) was used as a marker to track and observe the myelination using whole-mount in situ hybridization.RESULTS: Targeted knockdown of TNF-α resulted in specific suppression of TNF-α expression and a severely underdeveloped liver. The co-injection of TNF-α MO and m RNA rescued the liver development. Retinal neurogenesis in TNF-α morphants was initiated on time.The retina was fully laminated, while ganglion cells,cones, and rods were well differentiated at 72 hours post-fertilization(hpf). mbp was expressed in Schwann cells in the lateral line nerves and cranial nerves from 3days post-fertilization(dpf) as well as in oligodendrocytes linearly along the hindbrain bundles and the spinal cord from 4 dpf, which closely resembled its endogenous profile.CONCLUSION: TNF-α is not an essential regulator for retinal neurogenesis and optic myelination. 展开更多
关键词 tumor necrosis factor-alpha RETINA NEUROGENESIS MYELINATION ZEBRAFISH
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