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m6A Regulates Neurogenesis and Neuronal Development by Modulating Histone Methyltransferase Ezh2
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作者 Junchen Chen Yi-Chang Zhang +8 位作者 Chunmin Huang Hui Shen Baofa Sun Xuejun Cheng Yu-Jie Zhang Yun-Gui Yang Qiang Shu Ying Yang Xuekun Li 《基因组蛋白质组与生物信息学报:英文版》 CAS CSCD 2019年第2期154-168,共15页
N6-methyladenosine (m6A),catalyzed by the methyltransferase complex consisting of Mettl3 and Mettl14,is the most abundant RNA modification in mRNAs and participates in diverse biological processes. However,the roles a... N6-methyladenosine (m6A),catalyzed by the methyltransferase complex consisting of Mettl3 and Mettl14,is the most abundant RNA modification in mRNAs and participates in diverse biological processes. However,the roles and precise mechanisms of m6A modification in regulating neuronal development and adult neurogenesis remain unclear. Here,we examined the function of Mettl3,the key component of the complex,in neuronal development and adult neurogenesis of mice. We found that the depletion of Mettl3 significantly reduced m6A levels in adult neural stem cells (aNSCs) and inhibited the proliferation of aNSCs. Mettl3 depletion not only inhibited neu-ronal development and skewed the differentiation of aNSCs more toward glial lineage,but also affected the morphological maturation of newborn neurons in the adult brain. m6A immunoprecip-itation combined with deep sequencing (MeRIP-seq) revealed that m6A was predominantly enriched in transcripts related to neurogenesis and neuronal development. Mechanistically,m6A was present on the transcripts of histone methyltransferase Ezh2,and its reduction upon Mettl3 knockdown decreased both Ezh2 protein expression and consequent H3K27me3 levels. The defects of neurogenesis and neuronal development induced by Mettl3 depletion could be rescued by Ezh2 overexpression. Collectively,our results uncover a crosstalk between RNA and histone modifica-tions and indicate that Mettl3-mediated m6A modification plays an important role in regulating neurogenesis and neuronal development through modulating Ezh2. 展开更多
关键词 N6-methyladenosine (m6A) Mettl3 NEUROGENESIS NEURONAL DEVELOPMENT EZH2
Pain inhibition through transplantation of fetal neuronal progenitors into the injured spinal cord in rats 预览
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作者 Chary M. Batista Eric D. Mariano +6 位作者 Camila S. Dale Alexandre F. Cristante Luiz R. Britto Jose P. Otoch Manoel J. Teixeira Matthias Morgalla Guilherme Lepski 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第11期2011-2019,共9页
Neuropathic pain after spinal cord injury(SCI) is a complex condition that responds poorly to usual treatments. Cell transplantation represents a promising therapy;nevertheless, the ideal cell type in terms of neuroge... Neuropathic pain after spinal cord injury(SCI) is a complex condition that responds poorly to usual treatments. Cell transplantation represents a promising therapy;nevertheless, the ideal cell type in terms of neurogenic potential and effectiveness against pain remains largely controversial. Here, we evaluated the ability of fetal neural stem cells(fNSC) to relieve chronic pain and, secondarily, their effects on motor recovery. Adult Wistar rats with traumatic SCI were treated, 10 days after injury, with intra-spinal injections of culture medium(sham) or fNSCs extracted from telencephalic vesicles(TV group) or the ventral medulla(VM group) of E/14 embryos. Sensory(von Frey filaments and hot plate) and motor(the Basso, Beattie,Bresnahan locomotor rating scale and inclined plane test) assessments were performed during 8 weeks. Thereafter, spinal cords were processed for immunofluorescence and transplanted cells were quantified by stereology. The results showed improvement of thermal hyperalgesia in the TV and VM groups at 4 and 5 weeks after transplantation, respectively. Moreover, mechanical allodynia improved in both the TV and VM groups at 8 weeks. No significant motor recovery was observed in the TV or VM groups compared with sham. Stereological analyses showed that ~70% of TV and VM cells differentiated into NeuN+ neurons,with a high proportion of enkephalinergic and GABAergic cells in the TV group and enkephalinergic and serotoninergic cells in the VM group. Our study suggests that neuronal precursors from TV and VM, once implanted into the injured spinal cord, maturate into different neuronal subtypes, mainly GABAergic, serotoninergic, and enkephalinergic, and all subtypes alleviate pain, despite no significant motor recovery. The study was approved by the Animal Ethics Committee of the Medical School of the University of S?o Paulo(protocol number 033/14) on March 4, 2016. 展开更多
关键词 spinal cord injuries chronic PAIN neural stem cells cell TRANSPLANTATION neuronal differentiation GABAERGIC NEURON serotoninergic NEURON enkephalinergic NEURON
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An efficient protocol of cryo-correlative light and electron microscopy for the study of neuronal synapses
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作者 Rong Sun Yun-Tao Liu +4 位作者 Chang-Lu Tao Lei Qi Pak-Ming Lau Z. Hong Zhou Guo-Qiang Bi 《生物物理学报:英文版》 CSCD 2019年第3期111-122,共12页
Cryo-electron tomography is an emerging electron microscopy technique for determining three? dimensional structures of cellular architectures near their native state at nanometer resolution, with a shortcoming of lack... Cryo-electron tomography is an emerging electron microscopy technique for determining three? dimensional structures of cellular architectures near their native state at nanometer resolution, with a shortcoming of lack of specific labels. Fluorescence light microscopy;on the other hand, specifically visualizes target cellular and molecular components with fluorescent labels, but islim 让 ed to a resolution oftens to hundreds nanometers. Combining the advantages of the two techniques, we have developed a cryo-correlative light and electron microscopy system. Our system consists a custom-designed cryo-chamber that allows for fluorescence imaging of frozen-hydrated samples, and an algorithm to achieve accurate correlation. W让h this system and our optimized protocol, high-quality tomograms of neuronal synapses labelled by specific fluorescent tags in cultured hippocampal neurons are obtained at high efficiency. 展开更多
关键词 Cryo-correlative light and ELECTRON MICROSCOPY Cryo-electron TOMOGRAPHY NEURONAL SYNAPSE
Differences in pathological changes between two rat models of severe traumatic brain injury 预览
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作者 Yi-Ming Song Yu Qian +6 位作者 Wan-Qiang Su Xuan-Hui Liu Jin-Hao Huang Zhi-Tao Gong Hong-Liang Luo Chuang Gao Rong-Cai Jiang 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第10期1796-1804,共9页
The rat high-impact free weight drop model mimics the diffuse axonal injury caused by severe traumatic brain injury in humans,while severe controlled cortical impact can produce a severe traumatic brain injury model u... The rat high-impact free weight drop model mimics the diffuse axonal injury caused by severe traumatic brain injury in humans,while severe controlled cortical impact can produce a severe traumatic brain injury model using precise strike parameters.In this study,we compare the pathological mechanisms and pathological changes between two rat severe brain injury models to identify the similarities and differences.The severe controlled cortical impact model was produced by an electronic controlled cortical impact device,while the severe free weight drop model was produced by dropping a 500 g free weight from a height of 1.8 m through a plastic tube.Body temperature and mortality were recorded,and neurological deficits were assessed with the modified neurological severity score.Brain edema and bloodbrain barrier damage were evaluated by assessing brain water content and Evans blue extravasation.In addition,a cytokine array kit was used to detect inflammatory cytokines.Neuronal apoptosis in the brain and brainstem was quantified by immunofluorescence staining.Both the severe controlled cortical impact and severe free weight drop models exhibited significant neurological impairments and body temperature fluctuations.More severe motor dysfunction was observed in the severe controlled cortical impact model,while more severe cognitive dysfunction was observed in the severe free weight drop model.Brain edema,inflammatory cytokine changes and cortical neuronal apoptosis were more substantial and blood-brain barrier damage was more focal in the severe controlled cortical impact group compared with the severe free weight drop group.The severe free weight drop model presented with more significant apoptosis in the brainstem and diffused blood-brain barrier damage,with higher mortality and lower repeatability compared with the severe controlled cortical impact group.Severe brainstem damage was not found in the severe controlled cortical impact model.These results indicate that the severe controlled cortical impact model is relat 展开更多
关键词 nerve REGENERATION severe traumatic brain INJURY animal model comparison free weight drop controlled cortical impact NEUROLOGICAL impairment NEUROINFLAMMATION blood-brain barrier damage neuronal apoptosis diffuse AXONAL INJURY BRAINSTEM INJURY neural REGENERATION
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Noise and delay sustained chimera state in small world neuronal network
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作者 TANG Jun ZHANG Juan +1 位作者 MA Jun LUO JinMing 《中国科学:技术科学英文版》 SCIE EI CAS CSCD 2019年第7期1134-1140,共7页
Chimera state in neuronal network means the coexistence of synchronized and desynchronized firing patterns. It attracts much attention recently due to its possible relevance to the phenomenon of unihemispheric sleep i... Chimera state in neuronal network means the coexistence of synchronized and desynchronized firing patterns. It attracts much attention recently due to its possible relevance to the phenomenon of unihemispheric sleep in mammals. In this paper, we search for chimera state in a noisy small-world neuronal network, in which the neurons are delayed coupled. We found both transient and permanent chimera state when time delay is close to a critical value. The chimera state occurs due to the competition between the synchronized and desynchronized patterns in the neuronal network. On the other hand, intermediate intensity of noise facilitates the occurrence of delay-sustained chimera states. Comparison between noise and delay shows that time delay is the key factor determining the chimera state, whereas noise is a subordinate one. 展开更多
关键词 DELAY noise CHIMERA STATE NEURONAL network
GPER agonist G1 suppresses neuronal apoptosis mediated by endoplasmic reticulum stress after cerebral ischemia/reperfusion injury 预览
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作者 Zi-Wei Han Yue-Chen Chang +5 位作者 Ying Zhou Hang Zhang Long Chen Yang Zhang Jun-Qiang Si Li Li 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第7期1221-1229,共9页
Studies have confirmed a strong association between activation of the endoplasmic reticulum stress pathway and cerebral ischemia/reperfusion(I/R)injury.In this study,three key proteins in the endoplasmic reticulum str... Studies have confirmed a strong association between activation of the endoplasmic reticulum stress pathway and cerebral ischemia/reperfusion(I/R)injury.In this study,three key proteins in the endoplasmic reticulum stress pathway(glucose-regulated protein 78,caspase-12,and C/EBP homologous protein)were selected to examine the potential mechanism of endoplasmic reticulum stress in the neuroprotective effect of G protein-coupled estrogen receptor.Female Sprague-Dawley rats received ovariectomy(OVX),and then cerebral I/R rat models(OVX+I/R)were established by middle cerebral artery occlusion.Immediately after I/R,rat models were injected with 100μg/kg E2(OVX+I/R+E2),or 100μg/kg G protein-coupled estrogen receptor agonist G1(OVX+I/R+G1)in the lateral ventricle.Longa scoring was used to detect neurobehavioral changes in each group.Infarct volumes were measured by 2,3,5-triphenyltetrazolium chloride staining.Morphological changes in neurons were observed by Nissl staining.Terminal dexynucleotidyl transferase-mediated nick end-labeling staining revealed that compared with the OVX+I/R group,neurological function was remarkably improved,infarct volume was reduced,number of normal Nissl bodies was dramatically increased,and number of apoptotic neurons in the hippocampus was decreased after E2 and G1 intervention.To detect the expression and distribution of endoplasmic reticulum stress-related proteins in the endoplasmic reticulum,caspase-12 distribution and expression were detected by immunofluorescence,and mRNA and protein levels of glucose-regulated protein 78,caspase-12,and C/EBP homologous protein were determined by polymerase chain reaction and western blot assay.The results showed that compared with the OVX+I/R group,E2 and G1 treatment obviously decreased mRNA and protein expression levels of glucose-regulated protein 78,C/EBP homologous protein,and caspase-12.However,the G protein-coupled estrogen receptor antagonist G15(OVX+I/R+E2+G15)could eliminate the effect of E2 on cerebral I/R injury.These results confirm t 展开更多
关键词 nerve REGENERATION cerebral ischemia/reperfusion injury ESTROGEN G protein-coupled ESTROGEN receptor G1 G15 endoplasmic reticulum stress glucose-regulated PROTEIN 78 caspase-12 C/EBP homologous PROTEIN neuronal apoptosis neural REGENERATION
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Effect of Gastrodin on Early Brain Injury and Neurological Outcome After Subarachnoid Hemorrhage in Rats
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作者 Xinzhi Wang Shuyue Li +4 位作者 Jinbang Ma Chuangang Wang Anzhong Chen Zhenxue Xin Jianjun Zhang 《神经科学通报:英文版》 SCIE CAS CSCD 2019年第3期461-470,共10页
Gastrodin is a phenolic glycoside that has been demonstrated to provide neuroprotection in preclinical models of central nervous system disease, but its effect in subarachnoid hemorrhage(SAH) remains unclear. In this ... Gastrodin is a phenolic glycoside that has been demonstrated to provide neuroprotection in preclinical models of central nervous system disease, but its effect in subarachnoid hemorrhage(SAH) remains unclear. In this study, we showed that intraperitoneal administration of gastrodin(100 mg/kg per day) significantly attenuated the SAH-induced neurological deficit, brain edema, and increased blood-brain barrier permeability in rats. Meanwhile, gastrodin treatment significantly reduced the SAHinduced elevation of glutamate concentration in the cerebrospinal fluid and the intracellular Ca2+ overload.Moreover, gastrodin suppressed the SAH-induced microglial activation, astrocyte activation, and neuronal apoptosis. Mechanistically, gastrodin significantly reduced the oxidative stress and inflammatory response, up-regulated the expression of nuclear factor erythroid 2–related factor2, heme oxygenase-1, phospho-Akt and B-cell lymphoma2, and down-regulated the expression of BCL2-associated X protein and cleaved caspase-3. Our results suggested that the administration of gastrodin provides neuroprotection against early brain injury after experimental SAH. 展开更多
关键词 SUBARACHNOID HEMORRHAGE GASTRODIN Early brain injury NEUROPROTECTION NEURONAL apoptosis
Up-Regulation of Trem2 Inhibits Hippocampal Neuronal Apoptosis and Alleviates Oxidative Stress in Epilepsy via the PI3K/Akt Pathway in Mice
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作者 Ai-Hua Liu Min Chu Yu-Ping Wang 《神经科学通报:英文版》 SCIE CAS CSCD 2019年第3期471-485,共15页
Epilepsy is a chronic and severe neurological disorder that has negative effects on the autonomous activities of patients. Functionally, Trem2(triggering receptor expressed on myeloid cells-2) is an immunoglobulin rec... Epilepsy is a chronic and severe neurological disorder that has negative effects on the autonomous activities of patients. Functionally, Trem2(triggering receptor expressed on myeloid cells-2) is an immunoglobulin receptor that affects neurological and psychiatric genetic diseases. Based on this rationale, we aimed to assess the potential role of Trem2 integration with the PI3 K/Akt pathway in epilepsy. We used microarray-based gene expression profiling to identify epilepsy-related differentially-expressed genes. In a mouse hippocampal neuron model of epilepsy, neurons were treated with lowMg^2+ extracellular fluid, and the protein and mRNA expression of Trem2 were determined. Using a gain-offunction approach with Trem2, neuronal apoptosis and its related factors were assessed by flow cytometry, RT-qPCR,and Western blot analysis. In a pilocarpine-induced epileptic mouse model, the malondialdehyde(MDA) and8-hydroxy-20-deoxyguanosine(8-OHdG) content and superoxide dismutase(SOD) and glutathione-peroxidase(GSH-Px) activity in the hippocampus were determined,and the protein expression of Trem2 was measured. In addition, the regulatory effect of Trem2 on the PI3 K/Akt pathway was analyzed by inhibiting this pathway in both the cell and mouse models of epilepsy. Trem2 was found to occupy a core position and was correlated with epilepsy.Trem2 was decreased in the hippocampus of epileptic miceand epileptic hippocampal neurons. Of crucial importance,overexpression of Trem2 activated the PI3 K/Akt pathway to inhibit neuronal apoptosis. Moreover, activation of the PI3 K/Akt pathway through over-expression of Trem2 alleviated oxidative stress, as shown by the increased expression of SOD and GSH-Px and the decreased expression of MDA and 8-OHdG. The current study defines the potential role of Trem2 in inhibiting the development of epilepsy, indicating that Trem2 up-regulation alleviates hippocampal neuronal injury and oxidative stress, and inhibits neuronal apoptosis in epilepsy by activating the PI3 K/Akt pathway. 展开更多
关键词 Trem2 EPILEPSY NEURONAL apoptosis PI3K/Akt pathway OXIDATIVE stress
Electroacupuncture promotes peripheral nerve regeneration after facial nerve crush injury and upregulates the expression of glial cell-derived neurotrophic factor 预览
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作者 Jing Fei Lin Gao +2 位作者 Huan-Huan Li Qiong-Lan Yuan Lei-Ji Li 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第4期673-682,共10页
The efficacy of electroacupuncture in the treatment of peripheral facial paralysis is known,but the specific mechanism has not been clarified.Glial cell-derived neurotrophic factor(GDNF)has been shown to protect neuro... The efficacy of electroacupuncture in the treatment of peripheral facial paralysis is known,but the specific mechanism has not been clarified.Glial cell-derived neurotrophic factor(GDNF)has been shown to protect neurons by binding to N-cadherin.Our previous results have shown that electroacupuncture could increase the expression of N-cadherin mRNA in facial neurons and promote facial nerve regeneration.In this study,the potential mechanisms by which electroacupuncture promotes nerve regeneration were elucidated through assessing the effects of electroacupuncture on GDNF and N-cadherin expression in facial motoneurons of rabbits with peripheral facial nerve crush injury.New Zealand rabbits were randomly divided into a normal group(normal control,n=21),injury group(n=45)and electroacupuncture group(n=45).Model rabbits underwent facial nerve crush injury only.Rabbits in the electroacupuncture group received facial nerve injury,and then underwent electroacupuncture at Yifeng(TE17),Jiache(ST6),Sibai(ST2),Dicang(ST4),Yangbai(GB14),Quanliao(SI18),and Hegu(LI4;only acupuncture,no electrical stimulation).The results showed that in behavioral assessments,the total scores of blink reflex,vibrissae movement,and position of apex nasi,were markedly lower in the EA group than those in the injury group.Hematoxylin-eosin staining of the right buccinator muscle of each group showed that the cross-sectional area of buccinator was larger in the electroacupuncture group than in the injury group on days 1,14 and 21 post-surgery.Toluidine blue staining of the right facial nerve tissue of each group revealed that on day 14 post-surgery,there was less axonal demyelination and fewer inflammatory cells in the electroacupuncture group compared with the injury group.Quantitative real time-polymerase chain reaction showed that compared with the injury group,N-cadherin mRNA levels on days 4,7,14 and 21 and GDNF mRNA levels on days 4,7 and 14 were significantly higher in the electroacupuncture group.Western blot assay displayed that compared wi 展开更多
关键词 NERVE REGENERATION FACIAL paralysis ELECTROACUPUNCTURE glial cell-derived neurotrophic factor N-cadherin crush injury neuronal apoptosis FACIAL neuron NERVE DEMYELINATION neural REGENERATION
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Rac GTPases: domain-specific functions in neuronal development 预览
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作者 Steffen Norgaard Roger Pocock 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第8期1367-1368,共2页
Understanding fundamental mechanisms governing axon outgrowth and guidance can inform the development of therapeutic strategies to restore neuronal function damaged though injury or disease. Axons navigate the extrace... Understanding fundamental mechanisms governing axon outgrowth and guidance can inform the development of therapeutic strategies to restore neuronal function damaged though injury or disease. Axons navigate the extracellular environment by responding to guidance cues that bind to cell surface receptors to relay information intracellularly via Rho GTPase family members, including the Rac GTPases. 展开更多
关键词 RAC GTPASES domain-specific FUNCTIONS NEURONAL DEVELOPMENT
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Fresh human amniotic membrane effectively promotes the repair of injured common peroneal nerve 预览
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作者 Zhong-Yuan Zhang Jin Yang +5 位作者 Zhen-Hai Fan Da-Li Wang Yu-Ying Wang Tao Zhang Li-Mei Yu Chang-Yin Yu 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第12期2199-2208,共10页
Suture and autologous nerve transplantation are the primary therapeutic measures for completely severed nerves. However, imbalances in the microenvironment and adhesion of surrounding tissues can affect the quality of... Suture and autologous nerve transplantation are the primary therapeutic measures for completely severed nerves. However, imbalances in the microenvironment and adhesion of surrounding tissues can affect the quality of nerve regeneration and repair. Previous studies have shown that human amniotic membrane can promote the healing of a variety of tissues. In this study, the right common peroneal nerve underwent a 5-mm transection in rats. Epineural nerve repair was performed using 10/0 non-absorbable surgical suture. The repair site was wrapped with a two-layer amniotic membrane with α-cyanoacrylate rapid medical adhesive after suture. Hindlimb motor function was assessed using footprint analysis. Conduction velocity of the common peroneal nerve was calculated by neural electrical stimulation. The retrograde axoplasmic transport of the common peroneal nerve was observed using fast blue BB salt retrograde fluorescent staining. Hematoxylin- eosin staining was used to detect the pathological changes of the common peroneal nerve sputum. The mRNA expression of axon regeneration-related neurotrophic factors and inhibitors was measured using real-time polymerase chain reaction. The results showed that the amniotic membrane significantly improved the function of the injured nerve;the toe spread function rapidly recovered, the nerve conduction velocity was restored, and the number of fast blue BB salt particles were increased in the spinal cord. The amniotic membrane also increased the recovery rate of the tibialis anterior muscle and improved the tissue structure of the muscle. Meanwhile, mRNA expression of nerve growth factor, growth associated protein-43, collapsin response mediator protein-2, and brain-derived neurotrophic factor recovered to near-normal levels, while Lingo-1 mRNA expression decreased significantly in spinal cord tissues. mRNA expression of glial-derived neurotrophic factor did not change significantly. Changes in mRNA levels were more significant in amniotic-membrane-wrapping-treated rats compared with 展开更多
关键词 NERVE REGENERATION human amniotic membrane AXONAL Schwann cells α-cyanoacrylate rapid medical adhesive NEURAL suture TIBIAL anterior muscle neuronal growth factor common PERONEAL NERVE injury NEURAL REGENERATION
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Rare inherited missense variants of POGZ associate with autism risk and disrupt neuronal development
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作者 Wenjing Zhao Jieqiong Tan +15 位作者 Tengfei Zhu Jianjun Ou Ying Li Lu Shen Huidan Wu Lin Han Yanling Liu Xiangbin Jia Ting Bai Honghui Li Xiaoyan Ke Jingping Zhao Xiaobing Zou Zhengmao Hu Hui Guo Kun Xia 《遗传学报:英文版》 SCIE CAS CSCD 2019年第5期247-257,共11页
Excess de novo likely gene-disruptive and missense variants within dozens of genes have been identified in autism spectrum disorder(ASD)and other neurodevelopmental disorders.However,many rare inherited missense varia... Excess de novo likely gene-disruptive and missense variants within dozens of genes have been identified in autism spectrum disorder(ASD)and other neurodevelopmental disorders.However,many rare inherited missense variants of these high-risk genes have not been thoroughly evaluated.In this study,we analyzed the rare missense variant burden of POGZ in a large cohort of ASD patients from the Autism Clinical and Genetic Resources in China(ACGC)and further dissected the functional effect of diseaseassociated missense variants on neuronal development.Our results showed a significant burden of rare missense variants in ASD patients compared to the control population(P=4.6×10-5,OR=3.96),and missense variants in ASD patients showed more severe predicted functional outcomes than those in controls.Furthermore,by leveraging published large-scale sequencing data of neurodevelopmental disorders(NDDs)and sporadic case reports,we identified 8 de novo missense variants of POGZ in NDD patients.Functional analysis revealed that two inherited,but not de novo,missense variants influenced the cellular localization of POGZ and failed to rescue the defects in neurite and dendritic spine development caused by Pogz knockdown in cultured mouse primary cortical neurons.Significantly,L1CAM,an autism candidate risk gene,is differentially expressed in POGZ deficient cell lines.Reduced expression of L1cam was able to partially rescue the neurite length defects caused by Pogz knockdown.Our study showed the important roles of rare inherited missense variants of POGZ in ASD risk and neuronal development and identified the potential downstream targets of POGZ,which are important for further molecular mechanism studies. 展开更多
关键词 AUTISM POGZ NEURONAL development MISSENSE VARIANTS
Cell-Type Identification in the Autonomic Nervous System
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作者 Di-Shi Liu Tian-Le Xu 《神经科学通报:英文版》 SCIE CAS CSCD 2019年第1期145-155,共11页
The autonomic nervous system controls various internal organs and executes crucial functions through sophisticated neural connectivity and circuits. Its dysfunction causes an imbalance of homeostasis and numerous huma... The autonomic nervous system controls various internal organs and executes crucial functions through sophisticated neural connectivity and circuits. Its dysfunction causes an imbalance of homeostasis and numerous human disorders. In the past decades, great efforts have been made to study the structure and functions of this system, but so far, our understanding of the classification of autonomic neuronal subpopulations remains limited and a precise map of their connectivity has not been achieved.One of the major challenges that hinder rapid progress in these areas is the complexity and heterogeneity of autonomic neurons. To facilitate the identification of neuronal subgroups in the autonomic nervous system, here we review the well-established and cutting-edge technologies that are frequently used in peripheral neuronal tracing and profiling, and discuss their operating mechanisms, advantages, and targeted applications. 展开更多
关键词 AUTONOMIC nervous system NEURONAL TRACING Genetic MARKER Molecular PROFILING CELL-TYPE diversity
Adipose-derived stem cells modified by BDNF gene rescue erectile dysfunction after cavernous nerve injury 预览
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作者 Mei Yang Jiang-Yang Sun +2 位作者 Cheng-Cheng Ying Yong Wang Yong-Lian Guo 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第1期120-127,共8页
Cavernous nerve injury is the main cause of erectile dysfunction following radical prostatectomy.The recovery of erectile function following radical prostatectomy remains challenging.Our previous studies found that in... Cavernous nerve injury is the main cause of erectile dysfunction following radical prostatectomy.The recovery of erectile function following radical prostatectomy remains challenging.Our previous studies found that injecting adipose-derived stem cells(ADSCs)into the cavernosa could repair the damaged cavernous nerves,but the erectile function of the treated rats could not be restored to a normal level.We evaluated the efficacy of ADSCs infected with a lentiviral vector encoding rat brain-derived neurotrophic factor(lenti-rBDNF)in a rat model of cavernous nerve injury.The rats were equally and randomly divided into four groups.In the control group,bilateral cavernous nerves were isolated but not injured.In the bilateral cavernous nerve injury group,bilateral cavernous nerves were isolated and injured with a hemostat clamp for 2 minutes.In the ADSCGFP and ADSCrBDNF groups,after injury with a hemostat clamp for 2 minutes,rats were injected with ADSCs infected with lenti-GFP(1×106 in 20μL)and lenti-rBDNF(1×106 in 20μL),respectively.Erectile function was assessed 4 weeks after injury by measuring intracavernosal pressures.Then,penile tissues were collected for histological detection and western blot assay.Results demonstrated that compared with the bilateral cavernous nerve injury group,erectile function was significantly recovered in the ADSCGFP and ADSCrBDNF groups,and to a greater degree in the ADSCrBDNF group.Neuronal nitric oxide synthase content in the dorsal nerves and the ratio of smooth muscle/collagen were significantly higher in the ADSCrBDNF and ADSCGFP groups than in the bilateral cavernous nerve injury group.Neuronal nitric oxide synthase expression was obviously higher in the ADSCrBDNF group than in the ADSCGFP group.These findings confirm that intracavernous injection with ADSCs infected with lenti-rBDNF can effectively improve erectile dysfunction caused by cavernous nerve injury.This study was approved by the Medical Animal Care and Welfare Committee of Wuhan University,China(approval No.2017-163 展开更多
关键词 adipose-derived stem cells brain-derived neurotrophic factor cavernous nerve injury erectile dysfunction INFECTION intracavernous injection lentiviral vector neuronal nitric oxide synthase radical prostatectomy
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Neurotoxicity of the pesticide rotenone on neuronal polarization:a mechanistic approach 预览
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作者 Mariano Bisbal Mónica Sanchez 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第5期762-766,共5页
Neurons are the most extensive and polarized cells that display a unique single long axon and multiple dendrites,which are compartments exhibiting structural and functional differences.Polarity occurs early in neurona... Neurons are the most extensive and polarized cells that display a unique single long axon and multiple dendrites,which are compartments exhibiting structural and functional differences.Polarity occurs early in neuronal development and it is maintained by complex subcellular mechanisms throughout cell life.A well-defined and controlled spatio-temporal program of cellular and molecular events strictly regulates the formation of the axon and dendrites from a non-polarized cell.This event is critical for an adequate neuronal wiring and therefore for the normal functioning of the nervous system.Neuronal polarity is very sensitive to the harmful effects of different factors present in the environment.In this regard,rotenone is a crystalline,colorless and odorless isoflavone used as insecticide,piscicide and broad spectrum pesticide commonly used earlier in agriculture.In the present review we will summarize the toxicity mechanism caused by this pesticide in different neuronal cell types,focusing on a particular biological mechanism whereby rotenone could impair neuronal polarization in cultured hippocampal neurons.Recent advances suggest that the inhibition of axonogenesis produced by rotenone could be related with its effect on microtubule dynamics,the actin cytoskeleton and their regulatory pathways,particularly affecting the small RhoGTPase RhoA.Unveiling the mechanism by which rotenone produces neurotoxicity will be instrumental to understand the cellular mechanisms involved in neurodegenerative diseases influenced by this environmental pollutant,which may lead to research focused on the design of new therapeutic strategies. 展开更多
关键词 ROTENONE environmental POLLUTANTS toxicity NEURONAL polarity RhoGTPase RhoA Lfc Arhgef1
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Early constraint-induced movement therapy affects behavior and neuronal plasticity in ischemia-injured rat brains 预览
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作者 Xi-Hua Liu Hong-Yan Bi +2 位作者 Jie Cao Shuo Ren Shou-Wei Yue 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第5期775-782,共8页
Constraint-induced movement therapy is an effective rehabilitative training technique used to improve the restoration of impaired upper extremity movement after stroke.However,whether constraint-induced movement thera... Constraint-induced movement therapy is an effective rehabilitative training technique used to improve the restoration of impaired upper extremity movement after stroke.However,whether constraint-induced movement therapy is more effective than conventional rehabilitation in acute or sub-acute stroke remains controversial.The aim of the present study was to identify the optimal time to start constraint-induced movement therapy after ischemic stroke and to explore the mechanisms by which constraint-induced movement therapy leads to post-stroke recovery.Sixty-four adult male Sprague-Dawley rats were randomly divided into four groups:sham-surgery group,cerebral ischemia/reperfusion group,early constraint-induced movement therapy group,and late constraint-induced movement therapy group.Rat models of left middle cerebral artery occlusion were established according to the Zea Longa line embolism method.Constraint-induced movement therapy was conducted starting on day 1 or day 14 in the early constraint-induced movement therapy and late constraint-induced movement therapy groups,respectively.To explore the effect of each intervention time on neuromotor function,behavioral function was assessed using a balance beam walking test before surgery and at 8 and 21 days after surgery.The expression levels of brain-derived neurotrophic factor,nerve growth factor and Nogo receptor were evaluated using real time-polymerase chain reaction and western blot assay to assess the effect of each intervention time.The results showed that the behavioral score was significantly lower in the early constraint-induced movement therapy group than in the cerebral ischemia/reperfusion and late constraint-induced movement therapy groups at 8 days.At 21 days,the scores had significantly decreased in the early constraint-induced movement therapy and late constraint-induced movement therapy groups.At 8 days,only mild pyknosis appeared in neurons of the ischemic penumbra in the early constraint-induced movement therapy group,which was distinctly better 展开更多
关键词 NERVE REGENERATION ischemic stroke rehabilitation constraint-induced movement therapy NERVE growth factors functional recovery neuronal plasticity real time-polymerase chain reaction western blot assay rats neural REGENERATION
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Rapid and Sparse Labeling of Neurons Based on the Mutant Virus-Like Particle of Semliki Forest Virus
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作者 Fan Jia Xutao Zhu +4 位作者 Pei Lv Liang Hu Qing Liu Sen Jin Fuqiang Xu 《神经科学通报:英文版》 SCIE CAS CSCD 2019年第3期378-388,共11页
Sparse labeling of neurons contributes to uncovering their morphology, and rapid expression of a fluorescent protein reduces the experiment range. To achieve the goal of rapid and sparse labeling of neurons in vivo, w... Sparse labeling of neurons contributes to uncovering their morphology, and rapid expression of a fluorescent protein reduces the experiment range. To achieve the goal of rapid and sparse labeling of neurons in vivo, we established a rapid method for depicting the fine structure of neurons at 24 h post-infection based on a mutant viruslike particle of Semliki Forest virus. Approximately 0.014 fluorescent focus-forming units of the mutant virus-like particle transferred enhanced green fluorescent protein into neurons in vivo, and its affinity for neurons in vivo was stronger than for neurons in vitro and BHK21(baby hamster kidney) cells. Collectively, the mutant virus-likeparticle provides a robust and convenient way to reveal the fine structure of neurons and is expected to be a helper virus for combining with other tools to determine their connectivity. Our work adds a new tool to the approaches for rapid and sparse labeling of neurons in vivo. 展开更多
关键词 Semliki Forest virus MUTANT virus-like particle RAPID LABELING SPARSE LABELING NEURONAL morphology
Treadmill training improves neurological deficits and suppresses neuronal apoptosis in cerebral ischemic stroke rats 预览
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作者 Li-Mei Cao Zhi-Qiang Dong +1 位作者 Qiang Li Xu Chen 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第8期1387-1393,共7页
RehabilNation training is believed to be beneficial to patients with stroke, but its molecular mechanism is still unclear. Rat models of cerebral ischemic stroke were established by middle cerebral artery occlusion/re... RehabilNation training is believed to be beneficial to patients with stroke, but its molecular mechanism is still unclear. Rat models of cerebral ischemic stroke were established by middle cerebral artery occlusion/reperfusion, and then received treadmill training of different intens让ies, twice a day for 30 minutes for 1 week. Low-intensity training was conducted at 5 m/min, with a 10-minute running, 10-minute rest, and 10-minute running cycle. In the moderate-intensity training, the intensity gradually increased from 5 m/min to 10 m/min in 5 minutes, with the same rest cycle as above. In high-intensity training, the intensity gradually increased from 5 m/min to 25 m/min in 5 minutes, with the same rest cycle as above. The Bederson scale was used to evaluate the improvement of motor function. Infarct volume was detected using 2,3,5-triphenyltetrazolium chloride staining. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining was applied to detect the apoptosis of nerve cells in brain tissue. Western blot assay was employed to analyze the activation of cyclic adenosine monophosphate (cAMP)/protein kinase A and Akt/glycogen synthase kinase-3卩 signaling pathways in rat brain tissue. All training intensities reduced the neurological deficit score, infarct volume, and apoptosis in nerve cells in brain tissue of stroke rats. Training intensities activated the cAMP/protein kinase A and Akt/glycogen synthase kinase-3 beta signaling pathways. This activation was more obvious with higher training intensities. These changes were reversed by intracerebroventricular injection of protein kinase A inhibitor Rp-cAMP. Our findings indicate that the neuroprotective effect of rehabilitation training is achieved via activation of the cAMP/ protein kinase A and Akt/glycogen synthase kinase-3 beta signaling pathways. This study was approved by the Ethics Committee of Animal Experimentation in Shanghai No. 8 Peoples Hospital, China. 展开更多
关键词 nerve REGENERATION ischemic stroke TREADMILL training neuronal DEFICIT apoptosis cyclic adenosine MONOPHOSPHATE protein kinase A GLYCOGEN synthase kinase-3^ NEUROPROTECTIVE effect neural REGENERATION
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Time-course pattern of neuronal loss and gliosis in gerbil hippocampi following mild, severe, or lethal transient global cerebral ischemia 预览
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作者 Tae-Kyeong Lee Hyunjung Kim +9 位作者 Minah Song Jae-Chul Lee Joon Ha Park Ji Hyeon Ahn Go Eun Yang Hyeyoung Kim Taek Geun Ohk Myoung Cheol Shin Jun Hwi Cho Moo-Ho Won 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第8期1394-1403,共10页
Transient ischemia in the whole brain leads to neuronal loss/death in vulnerable brain regions. The striatum, neocortex and hippocampus selectively loose specific neurons after transient ischemia. Just 5 minutes of tr... Transient ischemia in the whole brain leads to neuronal loss/death in vulnerable brain regions. The striatum, neocortex and hippocampus selectively loose specific neurons after transient ischemia. Just 5 minutes of transient ischemia can cause pyramidal neuronal death in the hippocampal cornu ammonis (CA) 1 field at 4 days after transient ischemia. In this study, we investigated the effects of 5-minute (mild), 15-minute (severe), and 20-minute (lethal) transient ischemia by bilateral common carotid artery occlusion (BCCAO) on behavioral change and neuronal death and gliosis (astrocytosis and microgliosis) in gerbil hippocampal subregions (CA1-3 region and dentate gyrus). We performed spontaneous motor activity test to evaluate gerbil locomotor activity, cresyl violet staining to detect cellular distribution, neuronal nuclei immunohistochemistry to detect neuronal distribution, and Fluoro-Jade B histofluorescence to evaluate neuronal death. We also conducted immunohistochemical staining for glial fibrillary acidic protein and ionized calcium-binding adapter molecule 1 (Ibal) to evaluate astrocytosis and microgliosis, respectively. Animals subjected to 20-minute BCCAO died in at least 2 days. BCCAO for 15 minutes led to pyramidal cell death in hippocampal CA1-3 region 2 days later and granule cell death in hippocampal de匚tate gyrus 5 days later. Similar results were not found in animals subjected to 5-minute BCCAO. Gliosis was much more rapidly and severely progressed in animals subjected to 15-minute BCCAO than in those subjected to 5- minute BCCAO. Our results indicate that neuronal loss in the hippocampal formation following transient ischemia is significantly different according to regions and severity of transient ischemia. The experimental protocol was approved by Institutional Animal Care and Use Committee (AICUC) of Kangwon National University (approval No. KW-180124-1) on May 22, 2018. 展开更多
关键词 TRANSIENT global brain ischemia delayed neuronal death GLIAL activation ischemic duration hippocampus spontaneous motor activity Mongolian GERBIL histology neural regeneration
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Role of axon resealing in retrograde neuronal death and regeneration after spinal cord injury 预览
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作者 William Rodemer Michael E.Selzer 《中国神经再生研究:英文版》 SCIE CAS CSCD 2019年第3期399-404,共6页
Spinal cord injury leads to persistent behavioral deficits because mammalian central nervous system axons fail to regenerate.A neuron's response to axon injury results from a complex interplay of neuron-intrinsic ... Spinal cord injury leads to persistent behavioral deficits because mammalian central nervous system axons fail to regenerate.A neuron's response to axon injury results from a complex interplay of neuron-intrinsic and environmental factors.The contribution of axotomy to the death of neurons in spinal cord injury is controversial because very remote axotomy is unlikely to result in neuronal death,whereas death of neurons near an injury may reflect environmental factors such as ischemia and inflammation.In lampreys, axotomy due to spinal cord injury results in delayed apoptosis of spinal-projecting neurons in the brain, beyond the extent of these environmental factors.This retrograde apoptosis correlates with delayed resealing of the axon,and can be reversed by inducing rapid membrane resealing with polyethylene glycol. Studies in mammals also suggest that polyethylene glycol may be neuroprotective,although the mechanism(s)remain unclear.This review examines the early,mechanical,responses to axon injury in both mammals and lampreys,and the potential of polyethylene glycol to reduce injury-induced pathology.Identifying the mechanisms underlying a neuron's response to axotomy will potentially reveal new therapeutic targets to enhance regeneration and functional recovery in humans with spinal cord injury. 展开更多
关键词 AXON resealing REGENERATION RETROGRADE NEURONAL death spinal cord injury sea LAMPREY PEG mitochondrial DYSFUNCTION calcium signaling
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