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Mice lacking perforin have improved regeneration of the injured femoral nerve

Neural Regeneration Research 2022年第8期17卷 1802-1808页

作者： Igor Jakovčevski Monika von Düring David Lutz Maja Vulović Mohammad Hamad Gebhard Reiss Eckart Förster melitta schachner Institut für Anatomie und Klinische Morphologie Universität Witten/HerdeckeWittenGermany Department of Neuroanatomy and Molecular Brain Research Ruhr University BochumBochumGermany Department of Anatomy Faculty of Medical SciencesUniversity of KragujevacKragujevacSerbia Keck Center for Collaborative Neuroscience and Department of Cell Biology and Neuroscience Rutgers UniversityPiscatawayNJUSA

The role that the immune system plays after injury of the peripheral nervous system is still not completely understood.Perforin,a natural killer cell-and T-lymphocyte-derived enzyme that mediates cytotoxicity,plays important roles in autoimmune diseases,infections and central nervous system trauma,such as spinal cord injury.To dissect the roles of this single component of the immune response to injury,we tested regeneration after femoral nerve injury in perforin-deficient(Pfp^(-/-))and wild-type control mice.Single frame motion analysis showed better motor recovery in Pfp^(-/-)mice compared with control mice at 4 and 8 weeks after injury.Retrograde tracing of the motoneuron axons regrown into the motor nerve branch demonstrated more correctly projecting motoneurons in the spinal cord of Pfp^(-/-)mice compared with wild-types.Myelination of regrown axons measured by g-ratio was more extensive in Pfp^(-/-)than in wild-type mice in the motor branch of the femoral nerve.Pfp^(-/-)mice displayed more cholinergic synaptic terminals around cell bodies of spinal motoneurons after injury than the injured wild-types.We histologically analyzed lymphocyte infiltration 10 days after surgery and found that in Pfp^(-/-)mice the number of lymphocytes in the regenerating nerves was lower than in wild-types,suggesting a closed blood-nerve barrier in Pfp^(-/-)mice.We conclude that perforin restricts motor recovery after femoral nerve injury owing to decreased survival of motoneurons and reduced myelination.

关键词： blood-nerve barrier femoral nerve injury locomotor recovery lymphocytes myelination NK-cells perforin reinnervation

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A Surgery Protocol for Adult Zebrafish Spinal Cord Injury

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Journal of Genetics and Genomics 2012年第9期39卷 481-487页

作者： Ping Fang Jin-Fei Lin Hong-Chao Pan Yan-Qin Shen melitta schachner Center for Neuroscience Shantou University Medical College 22 Xinling Road Shantou 515041 China

Adult zebrafish has a remarkable capability to recover from spinal cord injury,providing an excellent model for studying neuro-regeneration. Here we list equipment and reagents,and give a detailed protocol for complete transection of the adult zebrafish spinal cord. In this protocol,potential problems and their solutions are described so that the zebrafish spinal cord injury model can be more easily and reproducibly performed.In addition,two assessments are introduced to monitor the success of the surgery and functional recovery：one test to assess free swimming capability and the other test to assess extent of neuroregeneration by in vivo anterograde axonal tracing.In the swimming behavior test,successful complete spinal cord transection is monitored by the inability of zebrafish to swim freely for 1 week after spinal cord injury,followed by the gradual reacquisition of full locomotor ability within 6 weeks after injury.As a morphometric correlate,anterograde axonal tracing allows the investigator to monitor the ability of regenerated axons to cross the lesion site and increasingly extend into the gray and white matter with time after injury,confirming functional recovery.This zebrafish model provides a paradigm for recovery from spinal cord injury,enabling the identification of pathways and components of neuroregeneration.

关键词： Zebrafish Spinal cord injury Surgery Locomotor recovery Axonal regrowth

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A mimetic peptide of α2,6-sialyllactose promotes neuritogenesis

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Neural Regeneration Research 2020年第6期15卷 1058-1065页

作者： Shuang-Xi Chen Jia-Hui He Yong-Jian Mi Hui-Fan Shen melitta schachner Wei-Jiang Zhao Center for Neuroscience Shantou University Medical CollegeShantouGuangdong ProvinceChina Department of Neurology The First Affiliated Hospital of University of South ChinaHengyangHunan ProvinceChina Department of Neurology Chongqing Qijiang Renmin HospitalChongqingChina Keck Center for Collaborative Neuroscience and Department of Cell Biology and Neuroscience Rutgers UniversityPiscatawayNJUSA

Oxidative stress contributes to the pathogenesis of neurodegenerative diseases.With the aim to find reagents that reduce oxidative stress,a phage display library was screened for peptides mimicking a2,6-sialyllactose(6'-SL),which is known to beneficially influence neural functions.Using Sambucus nigra lectin,which specifically binds to 6'-SL,we screened a phage display library and found a peptide comprising identical sequences of 12 amino acids.Mimetic peptide,reverse peptide and scrambled peptide were tested for inhibition of 6'-SL binding to the lectin.Indeed,lectin binding to 6'-SL was inhibited by the most frequently identified mimetic peptide,but not by the reverse or scrambled peptides,showing that this peptide mimics 6'-SL.Functionally,mimetic peptide,but not the reverse or scrambled peptides,increased viability and expression of neural cell adhesion molecule L1 in SK-N-SH human neuroblastoma cells,and promoted survival and neurite outgrowth of cultured mouse cerebellar granule neurons challenged by H_20_2-induced oxidative stress.The combined results indicate that the 6'-SL mimetic peptide promotes neuronal survival and neuritogenesis,thus raising hopes for the treatment of neurodegenerative diseases.This study was approved by the Medical Ethics Committee of Shantou University Medical College,China(approval No.SUMC 2014-004)on February 20,2014.

关键词： central nervous system cerebellar granule neurons mimetic peptide neural cell adhesion molecule L1 neuritogenesis neurodegenerative disease neuronal survival oxidative stress phage display Sambucus nigra lectin α2,6-sialyllactose

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Induction of clusterin Expression by Neuronal Cell Death in Zebrafish

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Journal of Genetics and Genomics 2014年第11期41卷 583-589页

作者： Yun-Mi Jeong Tae-Eun Jin Jung-Hwa Choi Mi-Sun Lee Hyun-Taek Kim Kyu-Seok Hwang Doo-Sang Park Hyun-Woo Oh Joong-Kook Choi Vladimir Korzh melitta schachner Kwan-Hee You Cheol-Hee Kim Department of Biology Chungnam National University Korea Research Institute of Bioscience and Biotechnology Department of Biochemistry College of MedicineChungbuk National University Institute of Molecular and Cell Biology Agency for ScienceTechnology and Research Keck Center for Collaborative Neuroscience and Department of Cell Biology and Neuroscience Rutgers University Center for Neuroscience Shantou University Medical College

Clusterin, a protein associated with multiple functions, is expressed in a wide variety of mammalian tissues. Although clusterin is known to be involved in neurodegenerative diseases, ageing, and tumorigenesis, a detailed analysis of the consequences of gain- or loss-of- function approaches has yet to be performed to understand the underlying mechanisms of clusterin functions. Since clusterin levels change in neurological diseases, it is likely that clusterin contributes to cell death and degeneration in general. Zebrafish was investigated as a model system to study human diseases. During development, zebrafish clusterin was expressed in the notochord and nervous system. Embryonic overexpression of clusterin by mRNA microinjection did not affect axis formation, whereas its knock-down by anti-sense morpholino treatment resulted in neuronal cell death. To analyze the function of clusterin in neurodegeneration, a transgenic zebrafish was investigated, in which nitroreductase expression is regulated under the control of a neuron-specifc huC promoter which is active between the stages of early neuronal precursors and mature neurons. Nitroreductase turns metronidazole into a cytotoxic agent that induces cell death within 12 h. After metronidazole treatment, transgenic zebrafish showed neuron-specific cell death. Interestingly, we also observed a dramatic induction of clusterin expression in the brain and spinal cord in these fish, suggesting a direct or indirect role of clusterin in neuronal cell death and thus, more generally, in neurodegeneration.

关键词： Clusterin Neuronal cell death Neurodegeneration Zebrafish

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L1 is a potential marker for poorly-differentiated pancreatic neuroendocrine carcinoma

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World Journal of Gastroenterology 2006年第1期12卷 94-98页

作者： Jussuf T Kaifi Ulrich Zinnkann Emre F Yekebas Paulus G Schurr Uta Reichelt Robin Wachowiak Henning C Fiegel Susann Petri melitta schachner Jakob RIzbicki Department of General Visceral and Thoracic SurgeryUniversity Medical Center Hamburg-EppendorfHamburgGermany Institute for Pathology University Medical Center Hamburg-EppendorfHamburgGermany Department of Pediatric Surgery University Medical Center Hamburg-EppendorfHamburgGermany Center for Molecular Neurobiology University Medical Center Hamburg-EppendorfHamburgGermany

瞄准：在胰腺的神经内分泌肿瘤决定 L1 的表示并且相关它与这个肿瘤的分类。方法：我们回顾地在原发性瘤或转移的石蜡节上由免疫组织化学在胰腺的神经内分泌肿瘤的 63 种情况中分析了 L1 表示。染色被过氧化物酶技术对人的 L1 与单音的... 详细信息

瞄准：在胰腺的神经内分泌肿瘤决定 L1 的表示并且相关它与这个肿瘤的分类。方法：我们回顾地在原发性瘤或转移的石蜡节上由免疫组织化学在胰腺的神经内分泌肿瘤的 63 种情况中分析了 L1 表示。染色被过氧化物酶技术对人的 L1 与单音的同种细胞的抗体 UJ127.11 执行。所有肿瘤被分类根据分类同样区分得好的神经内分泌肿瘤和癌或糟糕区分的神经内分泌癌。结果：L1 在 5 被检测(7.9%) 63 个胰腺的神经内分泌肿瘤。(44.4%) 四 9 糟糕区分的癌表示了 L1。相反，仅仅(1.9%) 1 为 L1 54 个区分得好的肿瘤或癌是积极的。没有表示在正常胰腺的织物的 Langerhans 小岛房间被发现。生气桌子分析显示出在 L1 表示和胰(P<0.01 ) 的神经内分泌肿瘤的分类之间的一个重要协会。结论：L1 明确地在被知道有最糟的预后的糟糕区分的胰腺的神经内分泌癌被表示。L1 可能是为与胰腺的神经内分泌癌诊断的病人的风险预言的一个标记。

关键词：电势神经内分泌癌胰腺肿瘤细胞分化

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β1 Integrin mediated effects of tenascin-R domains EGFL and FN6-8 on neural stem /progenitor cell proliferation and differentiation in vitro

β1 Integrin mediated effects of tenascin-R domains EGFL and...

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中国神经科学学会第四次会员代表大会暨第八届全国学术会议

作者： melitta schachner Zentrum f Keck Centre for Collaborative Neuroscience and Department of Cell Biology and Neuroscience Rutgers UniversityPiscatawayNJ 08854USA

＜正＞Neural stem/progenitor cells（NSCs） have the capacity for self-renewal and differentiation into major classes of central nervous system cell types,such as neurons,astrocytes and oligodendrocytes.The determination of fate of NSCs appears to be regulated by both intrinsic and extrinsic factors.Mounting evidence has shown that extracellular matrix molecules contribute to NSC proliferation and differentiation as extrinsic factors.Here we explore the effects of the epidermal growth factor-like（EGFL） and fibronectin typeⅢhomogolous domains 6-8（FN6-8） of the extracellular matrix molecule tenascin-R on NSC proliferation and differentiation.Our results show that domain FN6-8 inhibited NSC proliferation and promoted NSCs differentiation into astrocytes and less into oligodendrocytes or neurons.The EGFL domain did not affect NSC proliferation,but promoted NSC differentiation into neurons and reduced NSC differentiation into astrocytes and oligodendrocytes.Treatment of NSCs withβ1 integrin function-blocking antibody resulted in attenuation of inhibition of the effect of FN6-8 on NSC proliferation.The influence of EGFL or FN6-8 on NSCs differentiation was inhibited byβ1 integrin antibody application,implicatingβ1 integrin in proliferation and differentiation induced by EGFL and FN6-8 mediated triggering of NSCs.

关键词： Tenascin-R neural stem/progenitor cell proliferation differentiation

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Amyloid precursor protein clusters at CNS nodes of Ranvier and causes an APPThr668 phosphorylation-dependent increase in Nav1.6 sodium channel currents

Amyloid precursor protein clusters at CNS nodes of Ranvier a...

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中国神经科学学会第四次会员代表大会暨第八届全国学术会议

作者： melitta schachner Gavin S.DAWE Department of Physiology Sino-German Neuroscience Institute of Dalian Medical UniversityDalian 116044China Zentrum fur Molekulare Neurobiologie University of HamburgHamburgGermany Department of Pharmacology Yong Loo Lin School of MedicineNational University of Singapore117597Singapore

＜正＞Objective Amyloid precursor protein（APP）,commonly associated with Alzheimer’s disease（AD）,marks axonal degeneration.But its physiological distribution and function along myelinated axons remain unknown.This work was to investigate the physiological distribution of APP and its function in modulating the expression of Nav1.6 sodium channel. Understanding the physiological roles of APP in axonal function may offer new insights into the processes by which abnormal processing of APP can contribute to the pathogenesis of AD.Methods Immunofluorescences were performed to detect the location of APP along myelinated axons;Western blots were analyzed to investigate the expression of APP and sodium channel in the central nervous system（CNS）;Co-immunoprecipitations were done to explore whether APP and sodium channel form a molecular complex;Co-expressed full length APP or its intracellular domain（AICD,Go proteinbinding domain,Fe65 binding domain,or C31 domain） with Nav 1.6 sodium channels into Xenopus oocytes to study the function of APP in modulation of Nav 1.6 currents using two-electrode voltage clamp technique;Compared conduction velocity and cell surface expression between WT and KO of APP and related APPThr668 phosphorylation site mice to elucidate further the mechanism of APP on modulation of Nav 1.6 sodium channels.Results Aaxonal APP forms a complex with Nav 1.6 and aggregates only specifically at the nodes of Ranvier of the central nervous system（CNS）,but not the peripheral nervous system（PNS）.Notably,coexpression of APP or its intracellular domains containing a VTPEER motif with Nav 1.6 sodium channels in Xenopus oocytes resulted in an increase in peak sodium currents,which was enhanced by APPT668E mutation and blocked by APPT668A mutation and inhibitors of CDK5 and JNKs.The cell surface expression of Nav 1.6 sodium channels in the white matter of spinal cord is decreased in APP,p35 and JNK3 null mice.Consistently, APP,p35 and JNK3 deficiency significantly reduce spinal conduction velocity.Conclusion APP acts as

关键词： APP sodium channels nodes of Ranvier phosphorylation

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Amyloid precursor protein clusters at CNS nodes of Ranvier and causes an APPThr668 phosphorylation-dependent increase in Nav1.6 sodium channel currents

Amyloid precursor protein clusters at CNS nodes of Ranvier a...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Toshitaka Futagawa Sashi Kesavapany melitta schachner Gavin S.Dawe Department of Clinical Research Singapore General HospitalSingapore Department of Biochemistry Yong Loo Lin School of MedicineNational University of SingaporeSingapore Department of Pharmacology and Department of Anatomy Yong Loo Lin School of MedicineNational University of SingaporeSingapore

＜正＞APP,commonly associated with Alzheimer’s disease,marks axonal degeneration.Its physiological distribution and function along myelinated axons remain unknown.We report that APP null and APP overexpressing transgenic（APPtg） mice show minor hypo- and hyper-myelination,respectively.Through axoglial interactions, APP aggregates at nodes of Ranvier（NORs） in the CNS.Notably,coexpression of APP or its intracellular domains containing a VTPEER motif with Navl.6 sodium channels in Xenopus oocytes resulted in an increase in peak sodium currents,which was enhanced by APPT668E mutation and blocked by APPT668A mutation and inhibitors of CDK5 and JNKs.The cell surface expression of Navl.6 sodium channels in the white matter of spinal cord is decreased in APP,p35 and JNK3 null mice.Consistently,APP,p35 and JNK3 deficiency significantly reduce spinal conduction velocity.Thus,APP acts as a novel component at CNS NORs,modulating Navl.6 sodium channels in an APPThr668 phosphorylation-dependent manner.

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朗飞结处神经突起生长抑制因子(英文)

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神经疾病与精神卫生 2008年第1期8卷 5-16,F0003页

作者： Du-Yu Nie Qi-Dong Hu Quan-Hong Ma melitta schachner Zhi-Cheng Xiao Institute of Molecular and Cell Biology Singapore Sino- Germany Center for Neuroscience Dalian Medical University Dalian China Zentrum fur Molekulare Neurobiologie University of Hamburg Hamburg Germany Department of Clinical Research Singapore General Hospital Singapore

朗飞结以及结侧区是有鞘轴突上的一些极化区域,越来越多的证据表明胶质细胞分泌的某些抑制中枢神经系统损伤后轴突再生过程中神经突起生长的分子如粘蛋白(tenascins)、硫酸软骨素蛋白聚糖(chondroitin sulphate pro-teoglycans)、髓鞘... 详细信息

朗飞结以及结侧区是有鞘轴突上的一些极化区域,越来越多的证据表明胶质细胞分泌的某些抑制中枢神经系统损伤后轴突再生过程中神经突起生长的分子如粘蛋白(tenascins)、硫酸软骨素蛋白聚糖(chondroitin sulphate pro-teoglycans)、髓鞘相关糖蛋白(myelin-associated glycopro-tein,MAG)、轴突生长抑制因子(Nogo)以及少突胶质细胞髓鞘糖蛋白(OMGP)等非常特异性的富集于朗飞结区域。这些分子在体外组织培养过程中显示出强烈的神经突起生长抑制作用。在一些基因无义突变的动物模型,能够观察到朗飞结处轴突的生长,表明这些抑制分子能够生理性地保持轴突的完整性并且阻止轴突间随机和错误的联结,然而,大部分的基因无义突变动物模型显示不出明显的中枢神经系统再生改善。这些被称为抑制因子的分子是否是神经再生失败的真正元凶这些抑制因子体内体外实验结果的不一致以及它们特异的定位分布让我们有理由对它们在其他生理作用和功能方面进行重新评价。考虑到轴突-胶质细胞相互作用的双向特性,本综述认为这些抑制因子不仅通过神经元上的受体信号通路调节轴突的极化、离子通道的功能以及轴突的分枝,另一方面轴突产生的化学分子也能反馈性的通过朗飞结区域寡突胶质细胞上的胶质细胞受体信号通路影响寡突胶质细胞的发育。

关键词：朗飞结神经突起生长抑制分子中枢神经系统再生

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Loss of cell adhesion molecule CHL1 improves homeostatic adaptation and survival in hypoxic stress

Loss of cell adhesion molecule CHL1 improves homeostatic ada...

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中国神经科学学会第十届全国学术会议

作者： Xin HUANG Jia SUN Weifang RONG Tong ZHAO Li-ying WU Kuiwu WU melitta schachner Zhi-Cheng XIAO Ling-ling ZHU Ming FAN Institute of Molecular and Clinical Medicine Kunming Medical College

Objective CHLl is a transmembrane cell adhesion molecule that is critical for brain development and in the maintenance of neural circuits in the adult.Recent studies revealed that CHLl has diverse roles and is involved in the regulation of recovery after spinal cord injury.CHLl expression was down-regulated in the cerebral cortex,hypothalamus and brain stem after induction of acute hypoxia.In the current study we sought to address the role of CHLl in regulating homeostasis responses to hypoxia using CHLl knockout(CHLl) mice.Results We found that,compared with the wild type littermates,CHLl mice showed a dramatically lower mortality rate and an augmented ventilatory response after they were subjected to acute hypoxia.Immunofluorescence staining revealed that CHLl was expressed in the carotid body(CB),the key oxygen sensor in rodents and CHLl expression level in CB as assayed by western blot was decreased after hypoxic exposure.The number of glomus cells and the expression of tyrosine hydroxylase(TH,a marker for glomus cells) in CB of CHLl mice appeared to be increased compared with CHL1mice.In addition,in the ex vivo carotid body preparation,hypoxia induced a significantly greater afferent nerve discharge in CHLl mice compared with the CHL1 mice.Furthermore,the arterial blood pressure and plasma catecholamine level of CHLl mice were also significantly higher than those of CHL1 mice.Conclusion Our findings first demonstrate that CHLl is a novel intrinsic factor that is involved in carotid body function and in the ventilatory response to acute hypoxia.

关键词： CHL1 acute hypoxia homeostatic adaptation survival

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