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Current status and future prospects of stem cell therapy in Alzheimer’s disease 预览
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作者 Fu-Qiang Zhang Jin-Lan Jiang +3 位作者 Jing-Tian Zhang Han Niu Xue-Qi Fu Lin-Lin Zeng 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第2期242-250,共9页
Alzheimer’s disease is a common progressive neurodegenerative disorder, pathologically characterized by the presence of β-amyloid plaques and neurofibrillary tangles. Current treatment approaches using drugs only al... Alzheimer’s disease is a common progressive neurodegenerative disorder, pathologically characterized by the presence of β-amyloid plaques and neurofibrillary tangles. Current treatment approaches using drugs only alleviate the symptoms without curing the disease, which is a serious issue and influences the quality of life of the patients and their caregivers. In recent years, stem cell technology has provided new insights into the treatment of neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Currently, the main sources of stem cells include neural stem cells, embryonic stem cells, mesenchymal stem cells, and induced pluripotent stem cells. In this review, we discuss the pathophysiology and general treatment of Alzheimer’s disease, and the current state of stem cell transplantation in the treatment of Alzheimer’s disease. We also assess future challenges in the clinical application and drug development of stem cell transplantation as a treatment for Alzheimer’s disease. 展开更多
关键词 Alzheimer's disease β-amyloid drug development embryonic STEM CELLS induced PLURIPOTENT STEM CELLS mesenchymal STEM CELLS nerve REGENERATION NEURAL REGENERATION NEURAL STEM CELLS NEURODEGENERATIVE disorders STEM cell therapy
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Outgrowth endothelial cells form a functional cerebral barrier and restore its integrity after damage 预览
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作者 Rais Reskiawan Abdulkadir Mansour Alwjwaj +2 位作者 Othman Ahmad Othman Kamini Rakkar Ulvi Bayraktutan 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第6期1071-1078,共8页
Breakdown of blood-brain barrier,formed mainly by brain microvascular endothelial cells(BMECs),represents the major cause of mortality during early phases of ischemic strokes.Hence,discovery of novel agents that can e... Breakdown of blood-brain barrier,formed mainly by brain microvascular endothelial cells(BMECs),represents the major cause of mortality during early phases of ischemic strokes.Hence,discovery of novel agents that can effectively replace dead or dying endothelial cells to restore blood-brain barrier integrity is of paramount importance in stroke medicine.Although endothelial progenitor cells(EPCs)represent one such agents,their rarity in peripheral blood severely limits their adequate isolation and therapeutic use for acute ischemic stroke which necessitate their ex vivo expansion and generate early EPCs and outgrowth endothelial cells(OECs)as a result.Functional analyses of these cells,in the present study,demonstrated that only OECs endocytosed DiI-labelled acetylated low-density lipoprotein and formed tubules on matrigel,prominent endothelial cell and angiogenesis markers,respectively.Further analyses by flow cytometry demonstrated that OECs expressed specific markers for sternness(CD34),immaturity(CD133)and endothelial cells(CD31)but not for hematopoietic cells(CD45).Like BMECs,OECs established an equally tight in vitro model of human BBB with astrocytes and pericytes,suggesting their capacity to form tight junctions.Ischemic injury mimicked by concurrent deprivation of oxygen and glucose(4 hours)or deprivation of oxygen and glucose followed by reperfusion(20 hours)affected both barrier integrity and function in a similar fashion as evidenced by decreases in transendothelial electrical resistance and increases in paracellular flux,respectively.Wound scratch assays comparing the vasculoreparative capacity of cells revealed that,compared to BMECs,OECs possessed a greater proliferative and directional migratory capacity.In a triple culture model of BBB established with astrocytes,pericytes and BMEC,exogenous addition of OECs effectively repaired the damage induced on endothelial layer in serum-free conditions.Taken together,these data demonstrate that OECs may effectively home to the site of vascular injury and re 展开更多
关键词 cell-based therapy endothelial progenitor cells ENDOTHELIUM ischemic stroke NEURODEGENERATION novel therapeutics outgrowth endothelial cells regenerative medicine stem cells translational medicine
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Transfer of mitochondria from mesenchymal stem cells derived from induced pluripotent stem cells attenuates hypoxia-ischemia-induced mitochondrial dysfunction in PC12 cells 预览
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作者 Yan Yang Gen Ye +5 位作者 Yue-Lin Zhang Hai-Wei He Bao-Qi Yu Yi-Mei Hong Wei You Xin Li 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第3期464-472,共9页
Mitochondrial dysfunction in neurons has been implicated in hypoxia-ischemia-induced brain injury.Although mesenchymal stem cell therapy has emerged as a novel treatment for this pathology,the mechanisms are not fully... Mitochondrial dysfunction in neurons has been implicated in hypoxia-ischemia-induced brain injury.Although mesenchymal stem cell therapy has emerged as a novel treatment for this pathology,the mechanisms are not fully understood.To address this issue,we first co-cultured 1.5×10^5 PC12 cells with mesenchymal stem cells that were derived from induced pluripotent stem cells at a ratio of 1:1,and then intervened with cobalt chloride(CoCl2)for 24 hours.Reactive oxygen species in PC12 cells was measured by Mito-sox.Mitochondrial membrane potential(ΔΨm)in PC12 cells was determined by JC-1 staining.Apoptosis of PC12 cells was detected by terminal deoxynucleotidal transferase-mediated dUTP nick end-labeling staining.Mitochondrial morphology in PC12 cells was examined by transmission electron microscopy.Transfer of mitochondria from the mesenchymal stem cells derived from induced pluripotent stem cells to damaged PC12 cells was measured by flow cytometry.Mesenchymal stem cells were induced from pluripotent stem cells by lentivirus infection containing green fluorescent protein in mitochondria.Then they were co-cultured with PC12 cells in Transwell chambers and treated with CoCl2 for 24 hours to detect adenosine triphosphate level in PC12 cells.CoCl2-induced PC12 cell damage was dose-dependent.Co-culture with mesenchymal stem cells significantly reduced apoptosis and restoredΔΨm in the injured PC12 cells under CoCl2 challenge.Co-culture with mesenchymal stem cells ameliorated mitochondrial swelling,the disappearance of cristae,and chromatin margination in the injured PC12 cells.After direct co-culture,mitochondrial transfer from the mesenchymal stem cells stem cells to PC12 cells was detected via formed tunneling nanotubes between these two types of cells.The transfer efficiency was greatly enhanced in the presence of CoCl2.More importantly,inhibition of tunneling nanotubes partially abrogated the beneficial effects of mesenchymal stem cells on CoCl2-induced PC12 cell injury.Mesenchymal stem cells reduced CoCl2-induced 展开更多
关键词 apoptosis brain injury HYPOXIA-ISCHEMIA INDUCED pluripotent STEM CELLS mesenchymal STEM CELLS MITOCHONDRIAL membrane potential MITOCHONDRIAL TRANSFER PC12 CELLS tunneling nanotubes
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Skeletal muscle-derived cells repair peripheral nerve defects in mice 预览
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作者 Zi-Xiang Chen Hai-Bin Lu +3 位作者 Xiao-Lei Jin Wei-Feng Feng Xiao-Nan Yang Zuo-Liang Qi 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第1期152-161,共10页
Skeletal muscle-derived cells have strong secretory function,while skeletal muscle-derived stem cells,which are included in muscle-derived cells,can differentiate into Schwann cell-like cells and other cell types.Howe... Skeletal muscle-derived cells have strong secretory function,while skeletal muscle-derived stem cells,which are included in muscle-derived cells,can differentiate into Schwann cell-like cells and other cell types.However,the effect of muscle-derived cells on peripheral nerve defects has not been reported.In this study,5-mm-long nerve defects were created in the right sciatic nerves of mice to construct a peripheral nerve defect model.Adult female C57BL/6 mice were randomly divided into four groups.For the muscle-derived cell group,muscle-derived cells were injected into the catheter after the cut nerve ends were bridged with a polyurethane catheter.For external oblique muscle-fabricated nerve conduit and polyurethane groups,an external oblique muscle-fabricated nerve conduit or polyurethane catheter was used to bridge the cut nerve ends,respectively.For the sham group,the sciatic nerves on the right side were separated but not excised.At 8 and 12 weeks post-surgery,distributions of axons and myelin sheaths were observed,and the nerve diameter was calculated using immunofluorescence staining.The number,diameter,and thickness of myelinated nerve fibers were detected by toluidine blue staining and transmission electron microscopy.Muscle fiber area ratios were calculated by Masson’s trichrome staining of gastrocnemius muscle sections.Sciatic functional index was recorded using walking footprint analysis at 4,8,and 12 weeks after operation.The results showed that,at 8 and 12 weeks after surgery,myelin sheaths and axons of regenerating nerves were evenly distributed in the muscle-derived cell group.The number,diameter,and myelin sheath thickness of myelinated nerve fibers,as well as gastrocnemius muscle wet weight and muscle area ratio,were significantly higher in the muscle-derived cell group compared with the polyurethane group.At 4,8,and 12 weeks post-surgery,sciatic functional index was notably increased in the muscle-derived cell group compared with the polyurethane group.These criteria of the muscle-derived cel 展开更多
关键词 MUSCLE NERVE conduit myokine NERVE REGENERATION NERVE REPAIR peripheral NERVE REGENERATION polyurethane catheter seed CELLS SKELETAL MUSCLE SKELETAL muscle-derived CELLS tissue-engineered NERVE
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Stroke gets in your eyes:stroke-induced retinal ischemia and the potential of stem cell therapy 预览
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作者 Chase Kingsbury Matt Heyck +2 位作者 Brooke Bonsack Jea-Young Lee Cesar V.Borlongan 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第6期1014-1018,共5页
Stroke persists as a global health and economic crisis,yet only two interventions to reduce stroke-induced brain injury exist.In the clinic,many patients who experience an ischemic stroke often further suffer from ret... Stroke persists as a global health and economic crisis,yet only two interventions to reduce stroke-induced brain injury exist.In the clinic,many patients who experience an ischemic stroke often further suffer from retinal ischemia,which can inhibit their ability to make a functional recovery and may diminish their overall quality of life.Despite this,no treatments for retinal ischemia have been developed.In both cases,ischemia-induced mitochondrial dysfunction initiates a cell loss cascade and inhibits endogenous brain repair.Stem cells have the ability to transfer healthy and functional mitochondria not only ischemic neurons,but also to similarly endangered retinal cells,replacing their defective mitochondria and thereby reducing cell death.In this review,we encapsulate and assess the relationship between cerebral and retinal ischemia,recent preclinical advancements made using in vitro and in vivo retinal ischemia models,the role of mitochondrial dysfunction in retinal ischemia pathology,and the therapeutic potential of stem cell-mediated mitochondrial transfer.Furthermore,we discuss the pitfalls in classic rodent functional assessments and the potential advantages of laser Doppler as a metric of stroke progression.The studies evaluated in this review highlight stem cell-derived mitochondrial transfer as a novel therapeutic approach to both retinal ischemia and stroke.Furthermore,we posit the immense correlation between cerebral and retinal ischemia as an underserved area of study,warranting exploration with the aim of these treating injuries together. 展开更多
关键词 laser Doppler MCAO mesenchymal stem cells mitochondrial network mitochondrial transfer ophthalmic artery optic nerve oxygen-glucose deprivation regenerative medicine retinal ganglion cells visual impairment
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Stem cell therapy for Parkinson’s disease:safety and modeling 预览
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作者 Theo Stoddard-Bennett Renee Reijo Pera 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第1期36-40,共5页
For decades,clinicians have developed medications and therapies to alleviate the symptoms of Parkinson’s disease,but no treatment currently can slow or even stop the progression of this localized neurodegeneration.Fo... For decades,clinicians have developed medications and therapies to alleviate the symptoms of Parkinson’s disease,but no treatment currently can slow or even stop the progression of this localized neurodegeneration.Fortunately,sparked by the genetic revolution,stem cell reprogramming research and the advancing capabilities of personalization in medicine enable forward-thinking to unprecedented patient-specific modeling and cell therapies for Parkinson’s disease using induced pluripotent stem cells(iPSCs).In addition to modeling Parkinson’s disease more accurately than chemically-induced animal models,patient-specific stem cell lines can be created,elucidating the effects of genetic susceptibility and sub-populations’differing responses to in vitro treatments.Sourcing cell therapy with iPSC lines provides ethical advantages because these stem cell lines do not require the sacrifice of human zygotes and genetically-specific drug trails can be tested in vitro without lasting damage to patients.In hopes of finally slowing the progression of Parkinson’s disease or re-establishing function,iPSC lines can ultimately be corrected with gene therapy and used as cell sources for neural transplantation for Parkinson’s disease.With relatively localized neural degeneration,similar to spinal column injury,Parkinson’s disease presents a better candidacy for cell therapy when compared to other diffuse degeneration found in Alzheimer’s or Huntington’s Disease.Neurosurgical implantation of pluripotent cells poses the risk of an innate immune response and tumorigenesis.Precautions,therefore,must be taken to ensure cell line quality before transplantation.While cell quality can be quantified using a number of assays,a yielding a high percentage of therapeutically relevant dopaminergic neurons,minimal de novo genetic mutations,and standard chromosomal structure is of the utmost importance.Current techniques focus on iPSCs because they can be matched with donors using human leukocyte antigens,thereby reducing the sever 展开更多
关键词 alpha SYNUCLEIN animal model cell therapy DOPAMINERGIC neurons induced PLURIPOTENT STEM CELLS NEURODEGENERATION Parksinson’s disease STEM CELLS
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Action of trichostatin A on Alzheimer’s disease-like pathological changes in SH-SY5Y neuroblastoma cells 预览
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作者 Li-Hua Li Wen-Na Peng +2 位作者 Yu Deng1 Jing-Jing Li Xiang-Rong Tian 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第2期293-301,共9页
The histone deacetylase inhibitor, trichostatin A, is used to treat Alzheimer’s disease and can improve learning and memory but its underlying mechanism of action is unknown. To determine whether the therapeutic effe... The histone deacetylase inhibitor, trichostatin A, is used to treat Alzheimer’s disease and can improve learning and memory but its underlying mechanism of action is unknown. To determine whether the therapeutic effect of trichostatin A on Alzheimer’s disease is associated with the nuclear factor erythroid 2-related factor 2(Nrf2) and Kelch-like epichlorohydrin-related protein-1(Keap1) signaling pathway, amyloid β-peptide 25–35(Aβ25–35) was used to induce Alzheimer’s disease-like pathological changes in SH-SY5 Y neuroblastoma cells. Cells were then treated with trichostatin A. The effects of trichostatin A on the expression of Keap1 and Nrf2 were detected by real-time quantitative polymerase chain reaction, western blot assays and immunofluorescence. Total antioxidant capacity and autophagy activity were evaluated by total antioxidant capacity assay kit and light chain 3-I/II levels, respectively. We found that trichostatin A increased cell viability and Nrf2 expression, and decreased Keap1 expression in SH-SY5 Y cells. Furthermore, trichostatin A increased the expression of Nrf2-related target genes, such as superoxide dismutase, NAD(P)H quinone dehydrogenase 1 and glutathione S-transferase, thereby increasing the total antioxidant capacity of SH-SY5 Y cells and inhibiting amyloid β-peptide-induced autophagy. Knockdown of Keap1 in SH-SY5 Y cells further increased trichostatin A-induced Nrf2 expression. These results indicate that the therapeutic effect of trichostatin A on Alzheimer’s disease is associated with the Keap1-Nrf2 pathway. The mechanism for this action may be that trichostatin A increases cell viability and the antioxidant capacity of SH-SY5 Y cells by alleviating Keap1-mediated inhibition Nrf2 signaling, thereby alleviating amyloid β-peptide-induced cell damage. 展开更多
关键词 Alzheimer's disease amyloid-β peptide autophagy KEAP1 signal neurocytotoxicity oxidative stress damage SH-SY5Y cells total antioxidant capacity transcription factor Nrf2 TSA
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Is there a relationship between dopamine and rhegmatogenous retinal detachment? 预览
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作者 Alessio Martucci Massimo Cesareo +5 位作者 Maria Dolores Pinazo-Durán Michela Di Pierro Matteo Di Marino Carlo Nucci Massimiliano Coletta Raffaele Mancino 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第2期311-314,共4页
Dopamine and its receptors have been widely studied in the neurological conditions and in the retina. In this study, we evaluated the possible role of dopamine in rhegmatogenous retinal detachment(RRD) by comparing th... Dopamine and its receptors have been widely studied in the neurological conditions and in the retina. In this study, we evaluated the possible role of dopamine in rhegmatogenous retinal detachment(RRD) by comparing the amount of 3,4-dihydroxyphenylacetic acid(DOPAC), a surrogate index of retinal dopamin levels, in the vitreous sample of patients affected by RRD with those affected by macular pucker and vitre ous hemorrhage. Our results showed that significantly higher levels of DOPAC were found in the vitreou sample of patients affected by RRD compared with those affected by vitreous hemorrhage and macula pucker(P = 0.002). Specifically, no trace of the substance was found in vitreous hemorrhage and macula pucker samples. A slightly significant positive correlation was found among DOPAC and post-operativ best corrected visual acuity(r = 0.470, P = 0.049). No correlation was found between DOPAC and the day elapsed between diagnosis and surgery(P = 0.317). For the first time our findings suggest that DOPAC i released in RRD, but not in other retinal diseases such as vitreous hemorrhage and macular pucker. More over, we showed a correlation between visual acuity outcome and the amount of DOPAC in the vitreous This might have a potential, although still unknown, implication in the pathogenesis of the disease and/o in the associated photoreceptors loss. This study was approved by the Ethics Committee of Rome Tor Ver gata University Hospital(R.S.92.10) on September 24, 2010. 展开更多
关键词 3 4-dihydroxyphenylacetic acid DOPAC DOPAMINE DOPAMINERGIC amacrine cells DOPAMINERGIC neurotoxicity MACULAR pucker oxidative stress PHOTORECEPTOR degeneration rhegmatogenous retinal DETACHMENT VITREOUS hemorrhage
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Endothelin increases the proliferation of rat olfactory mucosa cells 预览
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作者 Bertrand Bryche Audrey Saint-Albin +3 位作者 Claire Le Poupon Schlegel Christine Baly Patrice Congar Nicolas Meunier 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第2期352-360,共9页
The olfactory mucosa holds olfactory sensory neurons directly in contact with an aggressive environment. In order to maintain its integrity, it is one of the few neural zones which are continuously renewed during the ... The olfactory mucosa holds olfactory sensory neurons directly in contact with an aggressive environment. In order to maintain its integrity, it is one of the few neural zones which are continuously renewed during the whole animal life. Among several factors regulating this renewal, endothelin acts as an anti-apoptotic factor in the rat olfactory epithelium. In the present study, we explored whether endothelin could also act as a proliferative factor. Using primary culture of the olfactory mucosa, we found that an early treatment with endothelin increased its growth. Consistently, a treatment with a mixture of BQ123 and BQ788(endothelin receptor antagonists) decreased the primary culture growth without affecting the cellular death level. We then used combined approaches of calcium imaging, reverse transcriptase-quantitative polymerase chain reaction and protein level measurements to show that endothelin was locally synthetized by the primary culture until it reached confluency. Furthermore, in vivo intranasal instillation of endothelin receptor antagonists led to a decrease of olfactory mucosa cell expressing proliferating cell nuclear antigen(PCNA), a marker of proliferation. Only short-term treatment reduced the PCNA level in the olfactory mucosa cells. When the treatment was prolonged, the PCNA level was not statistically affected but the expression level of endothelin was increased. Overall, our results show that endothelin plays a proliferative role in the olfactory mucosa and that its level is dynamically regulated. This study was approved by the Comité d’éthique en expérimentation animale COMETHEA(COMETHEA C2 EA-45;protocol approval #12-058) on November 28, 2012. 展开更多
关键词 AUTOCRINE factor cell CULTURE cellular dynamics ENDOTHELIN OLFACTION OLFACTORY basal CELLS OLFACTORY epithelium OLFACTORY mucosa primary CULTURE
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Exosomes as mediators of neuron-glia communication in neuroinflammation 预览
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作者 María Pascual Francesc Ibánez Consuelo Guerri 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第5期796-801,共6页
In recent years,a type of extracellular vesicles named exosomes has emerged that play an important role in intercellular communication under physiological and pathological conditions.These nanovesicles (30–150 nm) co... In recent years,a type of extracellular vesicles named exosomes has emerged that play an important role in intercellular communication under physiological and pathological conditions.These nanovesicles (30–150 nm) contain proteins,RNAs and lipids,and their internalization by bystander cells could alter their normal functions.This review focuses on recent knowledge about exosomes as messengers of neuron-glia communication and their participation in the physiological and pathological functions in the central nervous system.Special emphasis is placed on the role of exosomes under toxic or pathological stimuli within the brain,in which the glial exosomes containing inflammatory molecules are able to communicate with neurons and contribute to the pathogenesis of neuroinflammation and neurodegenerative disorders.Given the small size and characteristics of exosomes,they can cross the blood-brain barrier and be used as biomarkers and diagnosis for brain disorders and neuropathologies.Finally,although the application potential of exosome is still limited,current studies indicate that exosomes represent a promising strategy to gain pathogenic information to identify therapeutically targets and biomarkers for neurological disorders and neuroinflammation. 展开更多
关键词 biomarkers EXOSOMES glial cells NEUROINFLAMMATION neuron-glia commuication neurons NEUROPATHOLOGY therapy
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一种度量细胞网络结构的方法 预览
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作者 张雨 刘芳 《中国组织工程研究》 CAS 北大核心 2020年第1期83-86,共4页
背景:在多细胞组成的生物体社会中,细胞之间的通讯必不可少。众多细胞之间相互通讯、相互联系,形成了一个复杂的细胞网络结构。对细胞网络结构相关属性值进行度量和评价,显得极其重要。目的:基于复杂网络,提出了一种细胞网络结构的度量... 背景:在多细胞组成的生物体社会中,细胞之间的通讯必不可少。众多细胞之间相互通讯、相互联系,形成了一个复杂的细胞网络结构。对细胞网络结构相关属性值进行度量和评价,显得极其重要。目的:基于复杂网络,提出了一种细胞网络结构的度量方法。方法:结合文献研究及实际应用,搭建细胞网络结构的度量框架,分别从细胞节点的度、细胞网络的度分布、细胞网络的平均路径长度、细胞网络的簇系数等方面对细胞网络结构进行度量。以某小型实验为例,进行了实例验证。结果与结论:细胞网络的度分布中,绝大部分细胞节点的度值比较小,只有较少量细胞节点的度值较高。细胞网络中细胞节点的度分布P(k)的幂律分布特点越是明显,则此细胞网络结构越是合理,细胞网络越正常;同时,许多细胞网络结构具有较小的平均路径长度。细胞网络的簇系数越大,表明该细胞网络具有较高的聚集特性。一般情况下,细胞网络结构越“紧密”,细胞网络结构的“集团化”特性越明显,细胞网络越正常。 展开更多
关键词 细胞 复杂网络 网络结构 度量 度分布 平均路径长度 簇系数
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Role of miR-124 in the regulation of retinoic acid-induced Neuro-2A cell differentiation 预览
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作者 Qun You Qiang Gong +3 位作者 Yu-Qiao Han Rou Pi Yi-Jie Du Su-Zhen Dong 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第6期1133-1139,共7页
Retinoic acid can cause many types of cells,including mouse neuroblastoma Neuro-2 A cells,to differentiate into neurons.However,it is still unknown whether microRNAs(miRNAs)play a role in this neuronal differentiation... Retinoic acid can cause many types of cells,including mouse neuroblastoma Neuro-2 A cells,to differentiate into neurons.However,it is still unknown whether microRNAs(miRNAs)play a role in this neuronal differentiation.To address this issue,real-time polymerase chain reaction assays were used to detect the expression of several differentiation-related miRNAs during the differentiation of retinoic acid-treated Neuro-2 A cells.The results revealed that miR-124 and miR-9 were upregulated,while miR-125 b was downregulated in retinoic acid-treated Neuro-2 A cells.To identify the miRNA that may play a key role,miR-124 expression was regulated by transfection of miRNA mimics or inhibitors.Morphological analysis results showed that inhibition of miR-124 expression reversed the effects of retinoic acid on neurite outgrowth.Moreover,miR-124 overexpression alone caused Neuro-2 A cells to differentiate into neurons,and its inhibitor could block this effect.These results suggest that miR-124 plays an important role in retinoic acid-induced differentiation of Neuro-2 A cells. 展开更多
关键词 IMMUNOFLUORESCENCE MAP2 micro RNA mi R-124 Neuro-2A cells neurite outgrowth neuronal differentiation OVEREXPRESSION real-time PCR retinoic acid
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Ligustilide protects PC12 cells from oxygen-glucose deprivation/reoxygenation-induced apoptosis via the LKB1-AMPK-mTOR signaling pathway 预览
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作者 Dan-Yang Zhao Dong-Dong Yu +1 位作者 Li Ren Guo-Rong Bi 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第3期473-481,共9页
Autophagy has been shown to have a protective effect against brain damage.Ligustilide(LIG)is a bioactive substance isolated from Ligusticum chuanxiong,a traditional Chinese medicine.LIG has a neuroprotective effect;ho... Autophagy has been shown to have a protective effect against brain damage.Ligustilide(LIG)is a bioactive substance isolated from Ligusticum chuanxiong,a traditional Chinese medicine.LIG has a neuroprotective effect;however,it is unclear whether this neuroprotective effect involves autophagy.In this study,PC12 cells were treated with 1×10^-5–1×10^-9 M LIG for 0,3,12 or 24 hours,and cell proliferation was evaluated using the 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium(MTS)assay.Treatment with 1×10^-6 M LIG for 3 hours had the greatest effect on cell proliferation,and was therefore used for subsequent experiments.PC12 cells were pre-treated with 1×10^-6 M LIG for 3 hours,cultured in 95%N2/5%CO2 in Dulbecco’s modified Eagle’s medium without glucose or serum for 4 hours,and then cultured normally for 16 hours,to simulate oxygen-glucose deprivation/reoxygenation(OGD/R).Cell proliferation was assessed with the MTS assay.Apoptosis was detected by flow cytometry.The expression levels of apoptosis-related proteins,Bcl-2 and Bax,autophagy-related proteins,Beclin 1 and microtubule-associated protein l light chain 3B(LC3-II),and liver kinase B1(LKB1)-5′-adenosine monophosphate-activated protein kinase(AMPK)-mammalian target of rapamycin(mTOR)signaling pathway-related proteins were assessed by western blot assay.Immunofluorescence staining was used to detect LC3-II expression.Autophagosome formation was observed by electron microscopy.LIG significantly decreased apoptosis,increased Bcl-2,Beclin 1 and LC3-II expression,decreased Bax expression,increased LC3-II immunoreactivity and the number of autophagosomes,and activated the LKB1-AMPK-mTOR signaling pathway in PC12 cells exposed to OGD/R.The addition of the autophagy inhibitor 3-methyladenine or dorsomorphin before OGD/R attenuated the activation of the LKB1-AMPK-mTOR signaling pathway in cells treated with LIG.Taken together,our findings show that LIG promotes autophagy and protects PC12 cells from apoptosis induced by 展开更多
关键词 AMPK apoptosis autophagy Bax Bcl-2 BECLIN 1 LC3-II LIGUSTILIDE mTOR PC12 cells
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Pluripotent stem cell derived inhibitory interneurons–principles and applications in health and disease 预览
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作者 Francesca Keefe Meng Li 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第2期251-252,共2页
Inhibitory interneurons are gamma-aminobutyric acid-ergic (GABAergic) nerve cells that act to maintain the appropriate excitation-inhibition balance, and synchronise the output of principle cells to generate rhythmic ... Inhibitory interneurons are gamma-aminobutyric acid-ergic (GABAergic) nerve cells that act to maintain the appropriate excitation-inhibition balance, and synchronise the output of principle cells to generate rhythmic patterns of firing (Kessaris et al., 2014). This critical role, along with their brain-wide distribution, has led to the implication of interneurons in many neuropathologies, including schizophrenia, autism, dystonia and epilepsies (Marín, 2012). 展开更多
关键词 CELLS ACT HAS LED
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Effect of stromal cell-derived factor-1/CXCR4 axis in neural stem cell transplantation for Parkinson’s disease 预览
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作者 Jiao-Tian Xu Yuan Qian +7 位作者 Wei Wang Xiao-Xiang Chen Yang Li Yu Li Zhi-Yong Yang Xiao-Bin Song Di Lu Xing-Li Deng 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第1期112-119,共8页
Previous studies have shown that neural stem cell transplantation has the potential to treat Parkinson’s disease,but its specific mechanism of action is still unclear.Stromal cell-derived factor-1 and its receptor,ch... Previous studies have shown that neural stem cell transplantation has the potential to treat Parkinson’s disease,but its specific mechanism of action is still unclear.Stromal cell-derived factor-1 and its receptor,chemokine receptor 4(CXCR4),are important regulators of cell migration.We speculated that the CXCR4/stromal cell-derived factor 1 axis may be involved in the therapeutic effect of neural stem cell transplantation in the treatment of Parkinson’s disease.A Parkinson’s disease rat model was injected with 6-hydroxydopamine via the right ascending nigrostriatal dopaminergic pathway,and then treated with 5μL of neural stem cell suspension(1.5×104/L)in the right substantia nigra.Rats were intraperitoneally injected once daily for 3 days with 1.25 mL/kg of the CXCR4 antagonist AMD3100 to observe changes after neural stem cell transplantation.Parkinson-like behavior in rats was detected using apomorphine-induced rotation.Immunofluorescence staining was used to determine the immunoreactivity of tyrosine hydroxylase,CXCR4,and stromal cell-derived factor-1 in the brain.Using quantitative real-time polymerase chain reaction,the mRNA expression of stromal cell-derived factor-1 and CXCR4 in the right substantia nigra were measured.In addition,western blot assays were performed to analyze the protein expression of stromal cell-derived factor-1 and CXCR4.Our results demonstrated that neural stem cell transplantation noticeably reduced apomorphine-induced rotation,increased the mRNA and protein expression of stromal cell-derived factor-1 and CXCR4 in the right substantia nigra,and enhanced the immunoreactivity of tyrosine hydroxylase,CXCR4,and stromal cell-derived factor-1 in the brain.Injection of AMD3100 inhibited the aforementioned effects.These findings suggest that the stromal cell-derived factor-1/CXCR4 axis may play a significant role in the therapeutic effect of neural stem cell transplantation in a rat model of Parkinson’s disease.This study was approved by the Animal Care and Use Committee of Kunming 展开更多
关键词 AMD3100 CORPUS STRIATUM CXCR4 neural stem cells Parkinson’s disease STROMAL cell-derived factor-1 substantia nigra
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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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Claudin-15 overexpression inhibits proliferation and promotes apoptosis of Schwann cells in vitro 预览
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作者 Jian-Nan Li Zhan Zhang +2 位作者 Guang-Zhi Wu Deng-Bing Yao Shu-Sen Cui 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第1期169-177,共9页
Our previous experiments have discovered that Claudin-15 was up-regulated in Schwann cells of the distal nerve stumps of rat models of sciatic nerve injury.However,how Claudin-15 affects Schwann cell function is still... Our previous experiments have discovered that Claudin-15 was up-regulated in Schwann cells of the distal nerve stumps of rat models of sciatic nerve injury.However,how Claudin-15 affects Schwann cell function is still unknown.This study aimed to identify the effects of Claudin-15 on proliferation and apoptosis of Schwann cells cultured in vitro and explore the underlying mechanisms.Primary Schwann cells were obtained from rats.Claudin-15 in Schwann cells was knocked down using siRNA(siRNA-1 group)compared with the negative control siRNA transfection group(negative control group).Claudin-15 in Schwann cells was overexpressed using pGV230-Claudin-15 plasmid(pGV230-Claudin-15 group).The pGV230 transfection group(pGV230 group)acted as the control of the pGV230-Claudin-15 group.Cell proliferation was analyzed with EdU assay.Cell apoptosis was analyzed with flow cytometric analysis.Cell migration was analyzed with Transwell inserts.The mRNA and protein expressions were analyzed with quantitative polymerase chain reaction assay and western blot assay.The results showed that compared with the negative control group,cell proliferation rate was up-regulated;p-AKT/AKT ratio,apoptotic rate,p-c-Jun/c-Jun ratio,mRNA expression of protein kinase C alpha,Bcl-2 and Bax were down-regulated;and mRNA expression of neurotrophins basic fibroblast growth factor and neurotrophin-3 were increased in the siRNA-1 group.No significant difference was found in cell migration between the negative control and siRNA-1 groups.Compared with the pGV230 group,the cell proliferation rate was down-regulated;apoptotic rate,p-c-Jun/c-Jun ratio and c-Fos protein expression increased;mRNA expression of protein kinase C alpha and Bax decreased;and mRNA expressions of neurotrophins basic fibroblast growth factor and neurotrophin-3 were up-regulated in the pGV230-Claudin-15 group.The above results demonstrated that overexpression of Claudin-15 inhibited Schwann cell proliferation and promoted Schwann cell apoptosis in vitro.Silencing of Claudin-15 had the re 展开更多
关键词 apoptosis Bax cell PROLIFERATION c-Jun Claudin-15 NERVE regeneration peripheral NERVE injury protein kinase C alpha Schwann cells Wallerian DEGENERATION
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Protective effects of organic extracts of Alpinia oxyphylla against hydrogen peroxide-induced cytotoxicity in PC12 cells 预览
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作者 Li-Hong Duan Meng Li +10 位作者 Chun-Bao Wang Qing-Mei Wang Quan-Quan Liu Wan-Feng Shang Ya-Jin Shen Zhuo-Hua Lin Tong-Yang Sun Zheng-Zhi Wu Ying-Hong Li Yu-Long Wang Xun Luo 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第4期682-689,共8页
Alpinia oxyphylla,a traditional herb,is widely used for its neuroprotective,antioxidant and memory-improving effects.However,the neuroprotective mechanisms of action of its active ingredients are unclear.In this study... Alpinia oxyphylla,a traditional herb,is widely used for its neuroprotective,antioxidant and memory-improving effects.However,the neuroprotective mechanisms of action of its active ingredients are unclear.In this study,we investigated the neuroprotective effects of various organic extracts of Alpinia oxyphylla on PC12 cells exposed to hydrogen peroxide-induced oxidative injury in vitro.Alpinia oxyphylla was extracted three times with 95%ethanol(representing extracts 1–3).The third 95%ethanol extract was dried and resuspended in water,and then extracted successively with petroleum ether,ethyl acetate and n-butanol(representing extracts 4–6).The cell counting kit-8 assay and microscopy were used to evaluate cell viability and observe the morphology of PC12 cells.The protective effect of the three ethanol extracts(at tested concentrations of 50,100 and 200μg/mL)against cytotoxicity to PC12 cells increased in a concentration-dependent manner.The ethyl acetate,petroleum ether and n-butanol extracts(each tested at 100,150 and 200μg/mL)had neuroprotective effects as well.The optimum effective concentration ranged from 50–200μg/mL,and the protective effect of the ethyl acetate extract was comparatively robust.These results demonstrate that organic extracts of Alpinia oxyphylla protect PC12 cells against apoptosis induced by hydrogen peroxide.Our findings should help identify the bioactive neuroprotective components in Alpinia oxyphylla. 展开更多
关键词 active INGREDIENTS ALPINIA oxyphylla apoptosis ethanol crude extract fraction hydrogen PEROXIDE nerve regeneration NEUROPROTECTIVE agent NEUROPROTECTIVE effects PC12 cells traditional HERB
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Protective effect of rhodioloside and bone marrow mesenchymal stem cells infected with HIF-1-expressing adenovirus on acute spinal cord injury 预览
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作者 Xiao-Qin Ha Bo Yang +3 位作者 Huai-Jing Hou Xiao-Ling Cai Wan-Yuan Xiong Xu-Pan Wei 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第4期690-696,共7页
Rhodioloside has been shown to protect cells from hypoxia injury,and bone marrow mesenchymal stem cells have a good effect on tissue repair.To study the effects of rhodioloside and bone marrow mesenchymal stem cells o... Rhodioloside has been shown to protect cells from hypoxia injury,and bone marrow mesenchymal stem cells have a good effect on tissue repair.To study the effects of rhodioloside and bone marrow mesenchymal stem cells on spinal cord injury,a rat model of spinal cord injury was established using the Infinite Horizons method.After establishing the model,the rats were randomly divided into five groups.Rats in the control group were intragastrically injected with phosphate buffered saline(PBS)(5μL).PBS was injected at 6 equidistant points around 5 mm from the injury site and at a depth of 5 mm.Rats in the rhodioloside group were intragastrically injected with rhodioloside(5 g/kg)and intramuscularly injected with PBS.Rats in the mesenchymal stem cell(MSC)group were intramuscularly injected with PBS and intramuscularly with MSCs(8×10^6/mL in a 50-μL cell suspension).Rats in the Ad-HIF-MSC group were intragastrically injected with PBS and intramuscularly injected with HIF-1 adenovirus-infected MSCs.Rats in the rhodioloside+Ad-HIF-MSC group were intramuscularly injected with MSCs infected with the HIF-1 adenovirus and intragastrically injected with rhodioloside.One week after treatment,exercise recovery was evaluated with a modified combined behavioral score scale.Hematoxylin-eosin staining and Pischingert’s methylene blue staining were used to detect any histological or pathological changes in spinal cord tissue.Levels of adenovirus IX and Sry mRNA were detected by real-time quantitative polymerase chain reaction and used to determine the number of adenovirus and mesenchymal stem cells that were transfected into the spinal cord.Immunohistochemical staining was applied to detect HIF-1 protein levels in the spinal cord.The results showed that:(1)compared with the other groups,the rhodioloside+Ad-HIF-MSC group exhibited the highest combined behavioral score(P<0.05),the most recovered tissue,and the greatest number of neurons,as indicated by Pischingert’s methylene blue staining.(2)Compared with the PBS group,HIF-1 pro 展开更多
关键词 acute spinal cord injury ADENOVIRUS ADENOVIRUS gene IX bone MARROW mesenchymal stem cells combined behavioral score scale HIF-1α NERVE regeneration NERVE repair RHODIOLA rosea SRY
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Regional brain susceptibility to neurodegeneration:what is the role of glial cells? 预览
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作者 Andrea Beatriz Cragnolini Giorgia Lampitella +4 位作者 Assunta Virtuoso Immacolata Viscovo Fivos Panetsos Michele Papa Giovanni Cirillo 《中国神经再生研究:英文版》 SCIE CAS CSCD 2020年第5期838-842,共5页
The main pathological feature of the neurodegenerative diseases is represented by neuronal death that represents the final step of a cascade of adverse/hostile events.Early in the neurodegenerative process,glial cells... The main pathological feature of the neurodegenerative diseases is represented by neuronal death that represents the final step of a cascade of adverse/hostile events.Early in the neurodegenerative process,glial cells (including astrocytes,microglial cells,and oligodendrocytes) activate and trigger an insidious neuroinflammatory reaction,metabolic decay,blood brain barrier dysfunction and energy impairment,boosting neuronal death.How these mechanisms might induce selective neuronal death in specific brain areas are far from being elucidated.The last two decades of neurobiological studies have provided evidence of the main role of glial cells in most of the processes of the central nervous system,from development to synaptogenesis,neuronal homeostasis and integration into,highly specific neuro-glial networks.In this mini-review,we moved from in vitro and in vivo models of neurodegeneration to analyze the putative role of glial cells in the early mechanisms of neurodegeneration.We report changes of transcriptional,genetic,morphological,and metabolic activity in astrocytes and microglial cells in specific brain areas before neuronal degeneration,providing evidence in experimental models of neurodegenerative disorders,including Parkinson’s and Alzheimer’s diseases.Understanding these mechanisms might increase the insight of these processes and pave the way for new specific glia-targeted therapeutic strategies for neurodegenerative disorders. 展开更多
关键词 ASTROCYTES GLIAL cells microglia NEURODEGENERATIVE diseases NEUROINFLAMMATION Parkinson's disease reactive GLIOSIS selective neuronal degeneration
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