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Mitochondrial transplantation confers protection against the effects of ischemic stroke by repressing microglial pyroptosis and promoting Neurogenesis

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Neural Regeneration Research 2024年第6期19卷 1325-1335页

作者： Li Sun Zhaoyan Zhao Jing Guo Yuan Qin Qian Yu Xiaolong Shi Fei Guo Haiqin Zhang Xude Sun Changjun Gao Qian Yang Department of Experimental Surgery The Second Affiliated Hospital of Air Force Medical University Department of Anesthesiology The Second Affiliated Hospital of Air Force Medical University

Transferring healthy and functional mitochondria to the lateral ventricles confers neuroprotection in a rat model of ischemia-reperfusion injury. Autologous mitochondrial transplantation is also beneficial in pediatric patients with cardiac ischemia-reperfusion injury. Thus, transplantation of functional exogenous mitochondria may be a promising therapeutic approach for ischemic disease. To explore the neuroprotective effect of mitochondria transplantation and determine the underlying mechanism in ischemic stroke, in this study we established a photo-thrombosis-induced mouse model of focal ischemia and administered freshly isolated mitochondria via the tail vein or to the injury site(in situ). Animal behavior tests, immunofluorescence staining, 2,3,5-triphenyltetrazolium chloride(TTC) staining, mRNA-seq, and western blotting were used to assess mouse anxiety and memory, cortical infarct area, pyroptosis, and Neurogenesis, respectively. Using bioinformatics analysis, western blotting, co-immunoprecipitation, and mass spectroscopy, we identified S100 calcium binding protein A9(S100A9) as a potential regulator of mitochondrial function and determined its possible interacting proteins. Interactions between exogenous and endogenous mitochondria, as well as the effect of exogenous mitochondria on recipient microglia, were assessed in vitro. Our data showed that:(1) mitochondrial transplantation markedly reduced mortality and improved emotional and cognitive function, as well as reducing infarct area, inhibiting pyroptosis, and promoting cortical Neurogenesis;(2) microglial expression of S100A9 was markedly increased by ischemic injury and regulated mitochondrial function;(3) in vitro, exogenous mitochondria enhanced mitochondrial function, reduced redox stress, and regulated microglial polarization and pyroptosis by fusing with endogenous mitochondria; and(4) S100A9 promoted internalization of exogenous mitochondria by the microglia, thereby amplifying their pro-proliferation and anti-inflammatory effects. Taken togeth

关键词： ischemic stroke microglia mitochondria transplantation Neurogenesis pyroptosis

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Oscillating field stimulation promotes Neurogenesis of neural stem cells through miR-124/Tal1 axis to repair spinal cord injury in rats

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Neural Regeneration Research 2023年第4期18卷 895-900页

作者： Chao Fang Jian Sun Jun Qian Cai-Liang Shen Department of Orthopedics&Spine Surgery The First Affiliated Hospital of Anhui Medical UniversityHefeiAnhui ProvinceChina Department of Orthopedics The Second Affiliated Hospital of Anhui Medical UniversityHefeiAnhui ProvinceChina

Spinal cord injury often leads to severe motor and sensory deficits,and prognosis using the currently available therapies remains poor.Therefore,we aimed to explore a novel therapeutic approach for improving the prognosis of spinal cord injury.In this study,we implanted oscillating field stimulation devices and transplanted neural stem cells into the thoracic region(T9–T10)of rats with a spinal cord contusion.Basso-Beattie-Bresnahan scoring revealed that oscillating field stimulation combined with neural stem cells transplantation promoted motor function recovery following spinal cord injury.In addition,we investigated the regulation of oscillating field stimulation on the miR-124/Tal1 axis in neural stem cells.Transfection of lentivirus was performed to investigate the role of Tal1 in Neurogenesis of neural stem cells induced by oscillating field stimulation.Quantitative reverse transcription-polymerase chain reaction,immunofluorescence and western blotting showed that oscillating field stimulation promoted Neurogenesis of neural stem cells in vitro and in vivo.Hematoxylin and eosin staining showed that oscillating field stimulation combined with neural stem cells transplantation alleviated cavities formation after spinal cord injury.Taking the results together,we concluded that oscillating field stimulation decreased miR-124 expression and increased Tal1 content,thereby promoting the Neurogenesis of neural stem cells.The combination of oscillating field stimulation and neural stem cells transplantation improved Neurogenesis,and thereby promoted structural and functional recovery after spinal cord injury.

关键词： miR-124 neural stem cell Neurogenesis oscillating field stimulation recovery spinal cord injury Tal1 tissue repair transplantation

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Role of the histone methyltransferases Ezh2 and Suv4-20h1/Suv4-20h2 in Neurogenesis

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Neural Regeneration Research 2023年第3期18卷 469-473页

作者： Christopher T.Rhodes Chin-Hsing Annie Lin Eunice Kennedy Shriver National Institute of Child Health and Human Development(NICHD) National Institutes of Health(NIH)BethesdaMDUSA Department of Integrative Biology University of Texas at San AntonioSan AntonioTXUSA University of Texas at San Antonio Neurosciences Institute San AntonioTXUSA

Mechanisms regulating Neurogenesis involve broad and complex processes that represent intriguing therapeutic targets in the field of regenerative medicine.One influential factor guiding neural stem cell proliferation and cellular differentiation during Neurogenesis are epigenetic mechanisms.We present an overview of epigenetic mechanisms including chromatin structure and histone modifications;and discuss novel roles of two histone modifiers,Ezh2 and Suv4-20h1/Suv4-20h2(collectively referred to as Suv4-20h),in neurodevelopment and Neurogenesis.This review will focus on broadly reviewing epigenetic regulatory components,the roles of epigenetic components during Neurogenesis,and potential applications in regenerative medicine.

关键词： adult Neurogenesis epigenetic Ezh2 histone co-regulation histone modification neurodevelopment Neurogenesis regenerative medicine Suv4-20h

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The gut microbiome:implications for Neurogenesis and neurological diseases

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Neural Regeneration Research 2022年第1期17卷 53-58页

作者： Cheng Liu Shang-Yu Yang Long Wang Fang Zhou Department of Healthcare Administration College of Medical and Health ScienceAsia UniversityTaichungTaiwanChina Department of Anesthesiology Renmin Hospital of Wuhan UniversityWuhanHubei ProvinceChina

There is an increasing recognition of the strong links between the gut microbiome and the brain,and there is persuasive evidence that the gut microbiome plays a role in a variety of physiological processes in the central nervous system.This review summarizes findings that gut microbial composition alterations are linked to hippocampal Neurogenesis,as well as the possible mechanisms of action;the existing literature suggests that microbiota influence neurogenic processes,which can result in neurological disorders.We consider this evidence from the perspectives of neuroinflammation,microbial-derived metabolites,neurotrophins,and neurotransmitters.Based on the existing research,we propose that the administration of probiotics can normalize the gut microbiome.This could therefore also represent a promising treatment strategy to counteract neurological impairment.

关键词： gut microbiota microbial-derived metabolites microbiota-gut-brain axis Neurogenesis neuroinflammation neurological diseases neurotrophins probiotics

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Significance of mitochondrial activity in Neurogenesis and neurodegenerative diseases

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Neural Regeneration Research 2022年第4期17卷 741-747页

作者： Serra Ozgen Judith Krigman Ruohan Zhang Nuo Sun Departments of Physiology and Cell Biology The Ohio State University Wexner Medical CenterColumbusOHUSA College of Medicine Graduate Research in the Department of NeuroscienceThe Ohio State UniversityColumbusOHUSA Dorothy M.Davis Heart and Lung Research Institute The Ohio State University Wexner Medical CenterColumbusOHUSA College of Pharmacy Department of Graduate ResearchThe Ohio State UniversityColumbusOHUSA

Mitochondria play a multidimensional role in the function and the vitality of the neurological system.From the generation of neural stem cells to the maintenance of neurons and their ultimate demise,mitochondria play a critical role in regulating our neural pathways'homeostasis,a task that is critical to our cognitive health and neurological well-being.Mitochondria provide energy via oxidative phosphorylation for the neurotransmission and generation of an action potential along the neuron's axon.This paper will first review and examine the molecular subtleties of the mitochondria's role in Neurogenesis and neuron vitality,as well as outlining the impact of defective mitochondria in neural aging.The authors will then summarize neurodegenerative diseases related to either Neurogenesis or homeostatic dysfunction.Because of the significant detriment neurodegenerative diseases have on the quality of life,it is essential to understand their etiology and ongoing molecular mechanics.The mitochondrial role in Neurogenesis and neuron vitality is essential.Dissecting and understanding this organelle's role in the genesis and homeostasis of neurons should assist in finding pharmaceutical targets for neurodegenerative diseases.

关键词： Alzheimer's disease autophagy mitochondria mitophagy neural stem cells neurodegenerative diseases Neurogenesis Parkin Parkinson's disease PINK1

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Loss-of-function of KMT5B leads to neurodevelopmental disorder and impairs neuronal development and Neurogenesis

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Journal of Genetics and Genomics 2022年第9期49卷 881-890页

作者： Guodong Chen Lin Han Senwei Tan Xiangbin Jia Huidan Wu Yingting Quan Qiumeng Zhang Bin Yu Zhengmao Hu Kun Xia Hui Guo Center of Medical Genetics School of Life SciencesCentral South UniversityChangshaHunan 421001China Chongqing Reproductive and Genetics Institute Chongqing Health Center for Women and ChildrenChongqing 400010China CAS Center for Excellence in Brain Science and Intelligences Technology(CEBSIT) Chinese Academy of SciencesShanghai 200030China Hunan Key Laboratory of Animal Models for Human Diseases ChangshaHunan 410078China

Autism spectrum disorder(ASD)is a group of neurodevelopmental disorders that cause severe social,communication,and behavioral problems.Recent studies show that the variants of a histone methyltransferase gene KMT5B cause neurodevelopmental disorders(NDDs),including ASD,and the knockout of Kmt5b in mice is embryonic lethal.However,the detailed genotype-phenotype correlations and functional effects of KMT5B in neurodevelopment are unclear.By targeted sequencing of a large Chinese ASD cohort,analyzing published genome-wide sequencing data,and mining literature,we curated 39 KMT5B variants identified from NDD individuals.A genotype-phenotype correlation analysis for 10 individuals with KMT5B pathogenic variants reveals common symptoms,including ASD,intellectual disability,languages problem,and macrocephaly.In vitro knockdown of the expression of Kmt5b in cultured mouse primary cortical neurons leads to a decrease in neuronal dendritic complexity and an increase in dendritic spine density,which can be rescued by expression of human KMT5B but not that of pathogenic de novo missense mutants.In vivo knockdown of the Kmt5b expression in the mouse embryonic cerebral cortex by in utero electroporation results in decreased proliferation and accelerated migration of neural progenitor cells.Our findings reveal essential roles of histone methyltransferase KMT5B in neuronal development,prenatal Neurogenesis,and neuronal migration.

关键词： KMT5B Autism spectrum disorder Neurodevelopmental disorder Neurogenesis Neuronal migration

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Rbm8a regulates Neurogenesis and reduces Alzheimer's disease-associated pathology in the dentate gyrus of 5×FAD mice

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Neural Regeneration Research 2024年第4期19卷 863-871页

作者： Chenlu Zhu Xiao Ren Chen Liu Yawei Liu Yonggang Wang Department of Neurology Lanzhou University Second Hospital Department of Neurology The First Affiliated Hospital of Nanchang University Department of Neurology Xiaogan City Central Hospital Health Service Department of the Guard Bureau of the General Office of the Central Committee of the Communist Party of China Headache Center Department of NeurologyBeijing Tiantan HospitalCapital Medical University

Alzheimer’s disease is a prevalent and debilitating neurodegenerative condition that profoundly affects a patient’s daily functioning with progressive cognitive decline,which can be partly attributed to impaired hippocampal Neurogenesis.Neurogenesis in the hippocampal dentate gyrus is likely to persist throughout life but declines with aging,especially in Alzheimer’s disease.Recent evidence indicated that RNA-binding protein 8A(Rbm8a)promotes the proliferation of neural progenitor cells,with lower expression levels observed in Alzheimer’s disease patients compared with healthy people.This study investigated the hypothesis that Rbm8a overexpression may enhance Neurogenesis by promoting the proliferation of neural progenitor cells to improve memory impairment in Alzheimer’s disease.Therefore,Rbm8a overexpression was induced in the dentate gyrus of 5×FAD mice to validate this hypothesis.Elevated Rbm8a levels in the dentate gyrus triggered Neurogenesis and abated pathological phenotypes(such as plaque formation,gliosis reaction,and dystrophic neurites),leading to ameliorated memory performance in 5×FAD mice.RNA sequencing data further substantiated these findings,showing the enrichment of differentially expressed genes involved in biological processes including Neurogenesis,cell proliferation,and amyloid protein formation.In conclusion,overexpressing Rbm8a in the dentate gyrus of 5×FAD mouse brains improved cognitive function by ameliorating amyloid-beta-associated pathological phenotypes and enhancing Neurogenesis.

关键词： Adora2a Alzheimer’s disease astrocyte cAMP signaling pathway dentate gyrus dystrophic neurites microglia Neurogenesis plaque Rbm8a

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Inhibition of Notch 1 signaling in the subacute stage after stroke promotes striatal astrocyte-derived Neurogenesis

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Neural Regeneration Research 2023年第8期18卷 1777-1781页

作者： Xiao-Zhu Hao Cheng-Feng Sun Lu-Yi Lin Chan-Chan Li Xian-Jing Zhao Min Jiang Yan-Mei Yang Zhen-Wei Yao Department of Radiology Huashan HospitalFudan UniversityShanghaiChina Institutes of Science and State Key Laboratory of Medical Neurobiology Fudan UniversityShanghaiChina

Inhibition of Notch1 signaling has been shown to promote astrocyte-derived Neurogenesis after stroke.To investigate the regulatory role of Notch1 signaling in this process,in this study,we used a rat model of stroke based on middle cerebral artery occlusion and assessed the behavior of reactive astrocytes post-stroke.We used theγ-secretase inhibitor N-[N-(3,5-diuorophenacetyl)-1-alanyl]-S-phenylglycine t-butylester(DAPT)to block Notch1 signaling at 1,4,and 7 days after injury.Our results showed that only administration of DAPT at 4 days after stroke promoted astrocyte-derived Neurogenesis,as manifested by recovery of white matter fiber bundle integrity on magnetic resonance imaging,which is consistent with recovery of neurologic function.These findings suggest that inhibition of Notch1 signaling at the subacute stage post-stroke mediates neural repair by promoting astrocyte-derived Neurogenesis.

关键词： astrocyte diffusion kurtosis imaging magnetic resonance imaging middle cerebral artery occlusion N-[N-(3 5-diuorophenacetyl)-1-alanyl]-Sphenylglycine t-butylester neural repair Neurogenesis neuron Notch1 signaling subacute stage

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Decellularized extracellular matrix and mesenchymal stem cells promote recovery in traumatic brain injury by synergistically enhancing Neurogenesis and attenuating neuroinflammation

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Journal of Materials Science & Technology 2023年第7期138卷 17-28页

作者： Xuewei Zhang Bixue Wang Hua Hong Ying Wang Jiashang Liu Changsheng Liu Xi Chen Key Laboratory for Ultrafine Materials of Ministry of Education Frontiers Science Center for Materiobiology and Dynamic ChemistryEngineering Research Center for Biomaterials of Ministry of EducationSchool of Materials Science and EngineeringEast China University of Science and TechnologyShanghai 200237China

Damaged neurons and harsh microenvironments contribute to the injury cascades following traumatic brain injury(TBI).Mesenchymal stem cell(MSC)therapy is considered a viable choice for brain in-jury treatment;however,its clinical use is hindered by limited engraftment,low survival ratio,and uncontrolled differentiation.Herein,the decellularized brain extracellular matrix(dBECM)was prepared through a new method as a delivery system for MSCs.dBECM-based hydrogel with favorable biochem-ical and biomechanical features provides a microenvironment for MSCs in nerve repair.The MSCs-encapsulated dBECM-based hydrogel is shown to improve neuron compensation and structural regen-eration,alleviate neuroinflammation,and promote M1-to-M2 polarization of microglia.Our results first demonstrate that the combination of dBECM and MSCs is a critical vehicle to promote TBI repair from Neurogenesis and immunoregulation,showing promise for the physiological recovery of neurogenic dis-eases and injuries.

关键词： ECM Stem cells Brain injury Neurogenesis Neuroinflammation

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Psychiatric risk gene transcription factor 4 preferentially regulates cortical interneuron Neurogenesis during early brain development

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The Journal of Biomedical Research 2022年第4期36卷 242-254页

作者： Yuanyuan Wang Liya Liu Mingyan Lin State Key Laboratory of Reproductive Medicine Nanjing Medical UniversityNanjingJiangsu 211166China Department of Neurobiology School of Basic Medical SciencesNanjing Medical UniversityNanjingJiangsu 211166China

Genetic variants within or near the transcription factor 4 gene(TCF4)are robustly implicated in psychiatric disorders including schizophrenia.However,the biological pleiotropy poses considerable obstacles to dissect the potential relationship between TCF4 and those highly heterogeneous diseases.Through integrative transcriptomic analysis,we demonstrated that TCF4 is preferentially expressed in cortical interneurons during early brain development.Therefore,disruptions of interneuron development might be the underlying contribution of TCF4 perturbation to a range of neurodevelopmental disorders.Here,we performed chromatin immunoprecipitation sequencing(ChIP-seq)of TCF4 on human medial ganglionic eminence-like organoids(hMGEOs)to identify genome-wide TCF4 binding sites,followed by integration of multi-omics data from human fetal brain.We observed preferential expression of the isoform TCF4-B over TCF4-A.De novo motif analysis found that the identified 5916 TCF4 binding sites are significantly enriched for the E-box sequence.The predicted TCF4 targets in general have positively correlated expression levels with TCF4 in the cortical interneurons,and are primarily involved in biological processes related to Neurogenesis.Interestingly,we found that TCF4 interacts with non-bHLH proteins such as FOS/JUN,which may underlie the functional specificity of TCF4 in hMGEOs.This study highlights the regulatory role of TCF4 in interneuron development and provides compelling evidence to support the biological rationale linking TCF4 to the developing cortical interneuron and psychiatric disorders.

关键词： transcription factor 4 hMGEOs cortical interneuron ChIP-seq Neurogenesis schizophrenia

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