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Potential physiological and pathological roles for axonal ryanodine receptors

Neural Regeneration Research 2023年第4期18卷 756-759页

作者： David P.Stirling Kentucky Spinal Cord Injury Research Center and Departments of Neurological Surgery Anatomical Sciences and NeurobiologyMicrobiology and ImmunologyUniversity of LouisvilleSchool of MedicineLouisvilleKYUSA

Clinical disability following trauma or disease to the spinal cord often involves the loss of vital white matter elements including axons and glia.Although excessive Cais an established driver of axonal degeneration,therapeutically targeting externally sourced Cato date has had limited success in both basic and clinical studies.Contributing factors that may underlie this limited success include the complexity of the many potential sources of Caentry and the discovery that axons also contain substantial amounts of stored Cathat if inappropriately released could contribute to axonal demise.Axonal Castorage is largely accomplished by the axoplasmic reticulum that is part of a continuous network of the endoplasmic reticulum that provides a major sink and source of intracellular Cafrom the tips of dendrites to axonal terminals.This“neuron-within-a-neuron”is positioned to rapidly respond to diverse external and internal stimuli by amplifying cytosolic Calevels and generating short and long distance regenerative Cawaves through Cainduced Carelease.This review provides a glimpse into the molecular machinery that has been implicated in regulating ryanodine receptor mediated Carelease in axons and how dysregulation and/or overstimulation of these internodal axonal signaling nanocomplexes may directly contribute to Ca-dependent axonal demise.Neuronal ryanodine receptors expressed in dendrites,soma,and axonal terminals have been implicated in synaptic transmission and synaptic plasticity,but a physiological role for internodal localized ryanodine receptors remains largely obscure.Plausible physiological roles for internodal ryanodine receptors and such an elaborate internodal binary membrane signaling network in axons will also be discussed.

关键词： axomyelinic synapse axon axoplasmic reticulum calcium ryanodine receptor secondary axonal degeneration spinal cord injury voltage-gated calcium channel white matter injury

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Circulating immune cell landscape in patients who had mild ischaemic stroke

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stroke.& Vascular Neurology 2022年第4期7卷 319-327,I0020-I0022页

作者： Young-Eun Cho Hyangkyu Lee Heekyong R.Bae Hyungsuk Kim Sijung Yun Rany Vorn Ann Cashion Mary Jo Rucker Mariam Afzal Lawrence Latour Jessica Gill College of Nursing The University of IowaIowa CityIowaUSA national institute of Nursing Research National Institutes of HealthBethesdaMarylandUSA Mo-Im Kim Nursing Research institute College of NursingYonsei UniversitySeoulSouth Korea national Eye institute National Institutes of HealthBethesdaMarylandUSA Predictiv Care IncSunnyvaleCaliforniaUSA School of Nursing Johns Hopkins UniversityBaltimoreMarylandUSA College of Nursing University of Tennessee Health Science CenterMemphisTennesseeUSA Suburban Hospital BethesdaMarylandUSA national institute of Neurological disorders and stroke National Institutes of HealthBethesdaMarylandUSA

Introduction Patients who had a mild ischaemic stroke.who present with subtle or resolving symptoms sometimes go undiagnosed,are excluded from treatment and in some cases clinically worsen.Circulating immune cells are potential biomarkers that can assist with diagnosis in ischaemic stroke.Understanding the transcriptomic changes of each cell population caused by ischaemic stroke.is critical because they work closely in a complicated relationship.In this study,we investigated peripheral blood mononuclear cells(PBMCs)transcriptomics of patients who had a stroke.using a single-cell RNA sequencing to understand peripheral immune response after mild stroke.based on the gene expression in an unbiased way.Methods Transcriptomes of PBMCsfrom 10 patients who had an acute ischaemic stroke.within 24 hours after stroke.onset were compared with 9 race-matched/age-matched/gender-matched controls.Individual PBMCs were prepared with ddSeqTM(Illumina-BioRad)and sequenced on the Illumina NovaSeq 6000 platform.Results Notable population changes were observed in patients who had a stroke.especially in NK cells and CD14+monocytes.The number of NK cells was increased,which was further confirmed by flow cytometry.Functional analysis implied that the activity of NK cells also is enhanced in patients who had a stroke.CD14+monocytes were clustered into two groups;dendritic cell-related CD14+monocytes and NK cell-related CD14+monocytes.We found CD14+monocyte subclusters were dramatically reduced in patients who had a stroke.Discussion This is the first study demonstrating the increased number of NK cells and new monocyte subclusters of mild ischaemic stroke.based on the transcriptomic analysis.Our findings provide the dynamics of circulating immune response that could assist diagnosis and potential therapeutic development of mild ischaemic stroke.

关键词： patients diagnosis Circulating

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Large animal ischemic stroke.models: replicating human stroke.pathophysiology

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Neural Regeneration Research 2020年第8期15卷 1377-1387页

作者： Erin E.Kaiser Franklin D.West Regenerative Bioscience Center University of GeorgiaAthensGAUSA Neuroscience Program Biomedical and Health Sciences InstituteUniversity of GeorgiaAthensGAUSA Department of Animal and Dairy Science College of Agricultural and Environmental SciencesUniversity of GeorgiaAthensGAUSA

The high morbidity and mortality rate of ischemic stroke.in humans has led to the development of numerous animal models that replicate human stroke.to further understand the underlying pathophysiology and to explore potential therapeutic interventions.Although promising therapeutics have been identified using these animal models,with most undergoing significant testing in rodent models,the vast majority of these interventions have failed in human clinical trials.This failure of preclinical translation highlights the critical need for better therapeutic assessment in more clinically relevant ischemic stroke.animal models.Large animal models such as non-human primates,sheep,pigs,and dogs are likely more predictive of human responses and outcomes due to brain anatomy and physiology that are more similar to humans-potentially making large animal testing a key step in the stroke.therapy translational pipeline.The objective of this review is to highlight key characteristics that potentially make these gyrencephalic,large animal ischemic stroke.models more predictive by comparing pathophysiological responses,tissue-level changes,and model limitations.

关键词： brain ischemia clinical translation gyrencephalic large animal model magnetic resonance imaging stroke

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Gene expression profiles of human adipose-derived mesenchymal stem cells dynamically seeded on clinically available processed nerve allografts and collagen nerve guides

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Neural Regeneration Research 2021年第8期16卷 1613-1621页

作者： Femke Mathot Nadia Rbia Roman Thaler Allan B.Dietz Andre Jvan Wijnen Allen T.Bishop Alexander Y.Shin Department of Orthopedic Surgery Mayo ClinicRochesterMNUSA Department of Plastic Surgery RadboudumcNijmegenThe Netherlands Department of Dermatology Erasmus Medical CenterRotterdamThe Netherlands Department of Biochemistry and Molecular Biology Mayo ClinicRochesterMNUSA Department of Laboratory Medicine and Pathology Mayo ClinicRochesterMNUSA

It was hypothesized that mesenchymal stem cells(MSCs) could provide necessary trophic factors when seeded onto the surfaces of commonly used nerve graft substitutes. We aimed to determine the gene expression of MSCs when influenced by Avance■ Nerve Grafts or Neura Gen■ Nerve Guides. Human adipose-derived MSCs were cultured and dynamically seeded onto 30 Avance■ Nerve Grafts and 30 Neura Gen■ Nerve Guides for 12 hours. At six time points after seeding, quantitative polymerase chain reaction analyses were performed for five samples per group. Neurotrophic [nerve growth factor(NGF), glial cell line-derived neurotrophic factor(GDNF), pleiotrophin(PTN), growth associated protein 43(GAP43) and brain-derived neurotrophic factor(BDNF)], myelination [peripheral myelin protein 22(PMP22) and myelin protein zero(MPZ)], angiogenic [platelet endothelial cell adhesion molecule 1(PECAM1/CD31) and vascular endothelial cell growth factor alpha(VEGFA)], extracellular matrix(ECM) [collagen type alpha I(COL1A1), collagen type alpha III(COL3A1), Fibulin 1(FBLN1) and laminin subunit beta 2(LAMB2)] and cell surface marker cluster of differentiation 96(CD96) gene expression was quantified. Unseeded Avance■ Nerve Grafts and Neura Gen■ Nerve Guides were used to evaluate the baseline gene expression, and unseeded MSCs provided the baseline gene expression of MSCs. The interaction of MSCs with the Avance■ Nerve Grafts led to a short-term upregulation of neurotrophic(NGF, GDNF and BDNF), myelination(PMP22 and MPZ) and angiogenic genes(CD31 and VEGFA) and a long-term upregulation of BDNF, VEGFA and COL1A1. The interaction between MSCs and the Neura Gen■ Nerve Guide led to short term upregulation of neurotrophic(NGF, GDNF and BDNF) myelination(PMP22 and MPZ), angiogenic(CD31 and VEGFA), ECM(COL1A1) and cell surface(CD96) genes and long-term upregulation of neurotrophic(GDNF and BDNF), angiogenic(CD31 and VEGFA), ECM genes(COL1A1, COL3A1, and FBLN1) and cell surface(CD96) genes. Analysis demonstrated MSCs seeded onto Neura Gen■ Nerve Guides expr

关键词： Avance■Nerve Grafts dynamic seeding mesenchymal stem cell NeuraGen■Nerve Guides peripheral nerve repair qPCR

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父亲使用抗抑郁药物与子代结局:瑞典全国前瞻性队列研究

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英国医学杂志中文版 2022年第7期25卷 376-377页

作者： Alexander Viktorin Stephen Z Levine Margret Atemus Abraham Reichenberg Sven Sandin 李和程(译) 王忠(校) Departnent of Medical Epidemiology and Biostatistics Karolinska InstitutetStockholmSweden Department of Community Mental health University of HaifaHaifaIsrael Department of Psychiatry Yale School of MedicineNew HavenCTUSA Department of Psychiatry Icahn School of Medicine at Mount SinaiNew YorkNY 10029USA Seaver Autism Center for Research and Treatment at Mount Sinai New YorkNYUSA 西安交通大学第二附属医院泌尿外科上海交通大学医学院附属第九人民医院

目的探究父亲在母亲受孕期间使用抗抑郁药与子代早产、畸形、自闭症谱系障碍和智力残疾之间的关系。设计利用回归方法和阴性对照进行观察性前瞻性队列研究。研究地点瑞典全国。

关键词：前瞻性队列研究自闭症谱系障碍抗抑郁药物智力残疾回归方法观察性阴性对照子代

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Excitotoxicity, calcium and mitochondria: a triad in synaptic neurodegeneration

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Translational Neurodegeneration 2022年第1期11卷 917-930页

作者： Manish Verma Britney N.Lizama Charleen T.Chu Department of Pathology University of Pittsburgh School of MedicinePittsburghPA 15261USA Department of Ophthalmology University of Pittsburgh School of MedicinePittsburghPA 15261USA Pittsburgh institute for Neurodegenerative Diseases University of Pittsburgh School of MedicinePittsburghPA 15261USA McGowan institute for Regenerative Medicine University of Pittsburgh School of MedicinePittsburghPA 15261USA Center for Protein Conformational Diseases University of PittsburghPittsburghPA 15261USA Center for Neuroscience University of PittsburghPittsburghPA 15261USA Present Address:Astellas Pharma Inc. 9 Technology DriveWestboroughMA 01581USA.

Glutamate is the most commonly engaged neurotransmitter in the mammalian central nervous system,acting to mediate excitatory neurotransmission.However,high levels of glutamatergic input elicit excitotoxicity,contribut-ing to neuronal cell death following acute brain injuries such as stroke.and trauma.While excitotoxic cell death has also been implicated in some neurodegenerative disease models,the role of acute apoptotic cell death remains controversial in the setting of chronic neurodegeneration.Nevertheless,it is clear that excitatory synaptic dysregula-tion contributes to neurodegeneration,as evidenced by protective effects of partial N-methyl-D-aspartate receptor antagonists.Here,we review evidence for sublethal excitatory injuries in relation to neurodegeneration associated with Parkinson’s disease,Alzheimer’s disease,amyotrophic lateral sclerosis and Huntington’s disease.In contrast to classic excitotoxicity,emerging evidence implicates dysregulation of mitochondrial calcium handling in excitatory post-synaptic neurodegeneration.We discuss mechanisms that regulate mitochondrial calcium uptake and release,the impact of LRRK2,PINK1,Parkin,beta-amyloid and glucocerebrosidase on mitochondrial calcium transporters,and the role of autophagic mitochondrial loss in axodendritic shrinkage.Finally,we discuss strategies for normalizing the flux of calcium into and out of the mitochondrial matrix,thereby preventing mitochondrial calcium toxicity and excitotoxic dendritic loss.While the mechanisms that underlie increased uptake or decreased release of mitochondrial calcium vary in different model systems,a common set of strategies to normalize mitochondrial calcium flux can prevent excitatory mitochondrial toxicity and may be neuroprotective in multiple disease contexts.

关键词： Mitochondrial calcium Mitochondrial calcium uniporter NCLX antiporter Parkinson’s disease Alzheimer’s disease LRRK2 PINK1 Beta-amyloid Mitophagy Excitotoxicity Amyotrophic lateral sclerosis Huntington’s disease Glucocerebrosidase

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Open late:neuronal membrane disruption late in traumatic brain injury

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Neural Regeneration Research 2021年第12期16卷 2409-2410页

作者： Martina L.Hernandez MiJin Cho Audrey D.Lafrenaye Department of Anatomy and Neurobiology Virginia Commonwealth UniversityRichmondVAUSA

Membrane disruption is a pathology in which the cellular phospholipid bilayer,which is the cell’s primary defense from the extracellular environment,is compromised.Some neurons that are impacted by membrane disruption experience cell death,and others demonstrate delayed disruption,providing an opportunity for therapeutic intervention.

关键词： pathology traumatic disruption

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The role of vascularization in nerve regeneration of nerve graft

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Neural Regeneration Research 2020年第9期15卷 1573-1579页

作者： Tiam M.Saffari Meiwand Bedar Caroline A.Hundepool Allen T.Bishop Alexander Y.Shin Department of Orthopedic Surgery Mayo ClinicRochesterMNUSA Department of Plastic Reconstructive and Hand SurgeryErasmus Medical CenterRotterdamthe Netherlands

Vascularization is an important factor in nerve graft survival and function. The specific molecular regulations and patterns of angiogenesis following peripheral nerve injury are in a broad complex of pathways. This review aims to summarize current knowledge on the role of vascularization in nerve regeneration, including the key regulation molecules, and mechanisms and patterns of revascularization after nerve injury. Angiogenesis, the maturation of pre-existing vessels into new areas, is stimulated through angiogenic factors such as vascular endothelial growth factor and precedes the repair of damaged nerves. Vascular endothelial growth factor administration to nerves has demonstrated to increase revascularization after injury in basic science research. In the clinical setting, vascularized nerve grafts could be used in the reconstruction of large segmental peripheral nerve injuries. Vascularized nerve grafts are postulated to accelerate revascularization and enhance nerve regeneration by providing an optimal nutritional environment, especially in scarred beds, and decrease fibroblast infiltration. This could improve functional recovery after nerve grafting, however, conclusive evidence of the superiority of vascularized nerve grafts is lacking in human studies. A well-designed randomized controlled trial comparing vascularized nerve grafts to non-vascularized nerve grafts involving patients with similar injuries, nerve graft repair and follow-up times is necessary to demonstrate the efficacy of vascularized nerve grafts. Due to technical challenges, composite transfer of a nerve graft along with its adipose tissue has been proposed to provide a healthy tissue bed. Basic science research has shown that a vascularized fascial flap containing adipose tissue and a vascular bundle improves revascularization through excreted angiogenic factors, provided by the stem cells in the adipose tissue as well as by the blood supply and environmental support. While it was previously believed that revascularization occurred fro

关键词： angiogenesis fascial flap nerve graft nerve injury nerve regeneration peripheral nerve vascular endothelial growth factor vascularization vascularized nerve graft

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个体化循证医学:异质性治疗效应的预测方法

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英国医学杂志中文版 2019年第5期22卷 266-280页

作者： David M Kent Ewout Steyerberg David van Klaveren 周齐张静怡罗旭飞(译) 吕萌(译) 陈耀龙杨克虎(校) 张越伦(校) Predictive Analytics andComparative Effectiveness Center Institute for Clinical Research andHealth Policy StudiesTufts MedicalCenterBostonMA 02111USA Department of Biomedical DataSciences Leiden University MedicalCenterEinthovenweg 202333 ZCLeidenNetherlands 兰州大学循证医学中心兰州大学公共卫生学院北京协和医院中心实验室

使用来自临床试验的证据去支持个体患者决策是“参考类别预测”的一种形式:对个体的隐含预测是基于使用替代疗法治疗的“相似”患者参考类别的结果。循证医学普遍强调有资格的广泛参考类别患者参加试验。然而,试验(和临床实践)中的患者... 详细信息

使用来自临床试验的证据去支持个体患者决策是“参考类别预测”的一种形式:对个体的隐含预测是基于使用替代疗法治疗的“相似”患者参考类别的结果。循证医学普遍强调有资格的广泛参考类别患者参加试验。然而,试验(和临床实践)中的患者在许多方面彼此不同,这些可能影响主要的结局和潜在的获益。个体化医学各种形式的核心目标是缩小参考类别,以产生更多的患者特异性效应估计,从而支持更多个体化的临床决策。本文将回顾结果风险预测和治疗效应异质性(HTE)的基本概念问题,以及常规(单变量)亚组分析的局限性。讨论几种不同的基于回归的“预测性”HTE分析方法,包括基于“风险模型”(例如根据主要结局的风险或严重治疗相关危害的风险对试验人群进行分层)和“效应模型”的分析(其中包含相对效应的修饰)。用临床实例说明这些方法,并讨论它们各自的优势与不足。

关键词：个体化医学风险预测治疗效应循证医学异质性临床试验风险模型临床实践

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Effects of purposeful soccer heading on circulating small extracellular vesicle concentration and cargo

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Journal of Sport and health Science 2021年第2期10卷 122-130页

作者： Eric R.Munoz Jaclyn B.Caccese Brittany E.Wilson Kyle T.Shuler Fernando V.Santos Carolina T.Caban John J.Jeka Dianne Langford Matthew B.Hudson Department of Kinesiology and Applied Physiology University of DelawareNewarkDE 19713USA School of health and Rehabilitation Sciences The Ohio State University College of MedicineColumbusOH 43210USA Department of Neuroscience Lewis Katz School of MedicineTemple UniversityPhiladelphiaPA 19140USA

Background:Considering the potential cumulative effects of repetitive head impact(HI)exposure,we need sensitive biomarkers to track shortand long-term effects.Circulating small extracellular vesicles(sEVs)(healthy adult(aged 18-35 years)soccer players were randomly assigned to one of 3 groups:the HI group performed 10 standing headers,the leg impact group performed 10 soccer ball trapping maneuvers over 10 min,and the control group did not participate in any soccer drills.Plasma was collected before testing and 24 h afterward,and sEVs were isolated and characterized via nanoparticle tracking analysis.Next-generation sequencing was utilized to identify candidate miRNAs isolated from sEVs,and candidate microRNAs were analyzed via quantitative polymerase chain reaction.In silico target prediction was performed using TargetScan(Version 7.0;***)and miRWalk(http://mirwalk.***.uni-heidelberg.de/)programs,and target validation was performed using luciferase reporter vectors with a miR-7844-5p mimic in human embryonic kidney(HEK)293T/17 cells.Results:Plasma sEV concentration and size were not affected across time and group following repetitive HI exposure.After 24 h,the HI read count from next-generation sequencing showed a 4-fold or greater increase in miR-92b-5p,miR-423-5p,and miR-24-3p and a 3-fold or greater decrease in miR-7844-5p,miR-144-5p,miR-221-5p,and miR-22-3p.Analysis of quantitative polymerase chain reaction revealed that leg impact did not alter the candidate miRNA levels.To our knowledge,miR-7844-5p is a previously unknown miRNA.We identified 8 miR-7844-5p mRNA targets:protein phosphatase 1 regulatory inhibitor subunit 1B(PPP1R1B),LIM and senescent cell antigen-like domains 1(LIMS1),autophagy-related 12(ATG12),microtubule-associated protein 1

关键词： Biomarker Concussion MicroRNA Repetitive head impact exposure Soccer heading

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