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The combined application of stem cells and three-dimensional bioprinting scaffolds for the repair of spinal cord injury

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Neural Regeneration Research 2024年第8期19卷 1751-1758页

作者： Dingyue Ju Chuanming Dong Department of Anatomy Medical College of Nantong UniversityNantongJiangsu ProvinceChina key laboratory of neuroregeneration of jiangsu and Ministry of Education Co-innovation Center of NeuroregenerationNantong UniversityNantongJiangsu ProvinceChina

Spinal cord injury is considered one of the most difficult injuries to repair and has one of the worst prognoses for injuries to the nervous *** surgery,the poor regenerative capacity of nerve cells and the generation of new scars can make it very difficult for the impaired nervous system to restore its neural *** treatments can only alleviate secondary injuries but cannot fundamentally repair the spinal ***,there is a critical need to develop new treatments to promote functional repair after spinal cord *** recent years,there have been seve ral developments in the use of stem cell therapy for the treatment of spinal cord *** significant developments in the field of tissue engineering,three-dimensional bioprinting technology has become a hot research topic due to its ability to accurately print complex *** led to the loading of three-dimensional bioprinting scaffolds which provided precise cell *** three-dimensional bioprinting scaffolds co uld repair damaged neural circuits and had the potential to repair the damaged spinal *** this review,we discuss the mechanisms underlying simple stem cell therapy,the application of different types of stem cells for the treatment of spinal cord injury,and the different manufa cturing methods for three-dimensional bioprinting *** particular,we focus on the development of three-dimensional bioprinting scaffolds for the treatment of spinal cord injury.

关键词： biomaterials embryonic stem cells induced pluripotent stem cells mesenchymal stem cells nerve regeneration spinal cord injury stem cell therapy stem cells three-dimensional bioprinting

RNA sequencing of exosomes secreted by fibroblast and Schwann cells elucidates mechanisms underlying peripheral nerve regeneration

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Neural Regeneration Research 2024年第8期19卷 1812-1821页

作者： Xinyang Zhou Yehua Lv Huimin Xie Yan Li Chang Liu Mengru Zheng Ronghua Wu Songlin Zhou Xiaosong Gu Jingjing Li Daguo Mi Suzhou Medical College of Soochow University SuzhouJiangsu ProvinceChina key laboratory of neuroregeneration of jiangsu and Ministry of Education Co-Innovation Center of NeuroregenerationNantong UniversityNantongJiangsu ProvinceChina Department of Orthopedic Nantong Traditional Chinese Medicine HospitalNantongJiangsu ProvinceChina Nantong Stomatological Hospital Affiliated to Nantong University NantongJiangsu ProvinceChina Department of General Practice Affiliated Hospital of Nantong UniversityNantongJiangsu ProvinceChina

Exosomes exhibit complex biological functions and mediate a variety of biological processes,such as promoting axonal regeneration and functional recove ry after *** non-coding RNAs(IncRNAs)have been reported to play a crucial role in axonal *** r,the role of the IncRNA-microRNAmessenger RNA(mRNA)-competitive endogenous RNA(ceRNA)network in exosome-mediated axonal regeneration remains *** this study,we performed RNA transcriptome sequencing analysis to assess mRNA expression patterns in exosomes produced by cultured fibroblasts(FC-EXOs)and Schwann cells(SCEXOs).Diffe rential gene expression analysis,Gene Ontology analysis,Kyoto Encyclopedia of Genes and Genomes analysis,and protein-protein intera ction network analysis were used to explo re the functions and related pathways of RNAs isolated from FC-EXOs and *** found that the ribosome-related central gene Rps5 was enriched in FC-EXOs and SC-EXOs,which suggests that it may promote axonal *** addition,using the miRWalk and Starbase prediction databases,we constructed a regulatory network of ceRNAs targeting Rps5,including 27 microRNAs and five *** ceRNA regulatory network,which included Ftx and Miat,revealed that exsosome-derived Rps5 inhibits scar formation and promotes axonal regeneration and functional recovery after nerve *** findings suggest that exosomes derived from fibro blast and Schwann cells could be used to treat injuries of peripheral nervous system.

关键词： ceRNA network exosomes fibroblast cells Gene Ontology(GO) Kyoto Encyclopedia of Genes and Genomes(KEGG) protein-protein interaction(PPI)networks RNA-seq Schwann cells

Chemokine platelet factor 4 accelerates peripheral nerve regeneration by regulating Schwann cell activation and axon elongation

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Neural Regeneration Research 2024年第1期19卷 190-195页

作者： Miao Gu Xiao Cheng Di Zhang Weiyan Wu Yi Cao Jianghong He key laboratory of neuroregeneration of jiangsu and Ministry of Education Co-innovation Center of NeuroregenerationNMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology ProductsNantong UniversityNantongJiangsu ProvinceChina School of Basic Medical Sciences Hebei Key Laboratory of Nerve Injury and RepairChengde Medical UniversityChengdeHebei ProvinceChina

Schwann cells in peripheral nerves react to traumatic nerve injury by attempting to grow and *** r,it is unclear what factors play a role in this *** this study,we searched a GEO database and found that expression of platelet factor 4 was markedly up-regulated after sciatic nerve *** factor is an important molecule in cell apoptosis,diffe rentiation,survival,and ***,polymerase chain reaction and immunohistochemical staining confirmed the change in platelet factor 4 in the sciatic nerve at different time points after ***-linked immunosorbent assay confirmed that platelet factor 4 was secreted by Schwann *** also found that silencing platelet factor 4 decreased the proliferation and migration of primary cultured Schwann cells,while exogenously applied platelet factor 4 stimulated Schwann cell prolife ration and migration and neuronal axon ***,knocking out platelet factor 4 inhibited the prolife ration of Schwann cells in injured rat sciatic *** findings suggest that Schwann cell-secreted platelet factor 4 may facilitate peripheral nerve repair and regeneration by regulating Schwann cell activation and axon ***,platelet factor 4 may be a potential therapeutic target for traumatic peripheral nerve injury.

关键词： axon elongation bioinformatic analysis cell migration cell proliferation dorsal root ganglia peripheral nerve regeneration peripheral nerve trauma platelet factor 4 rat sciatic nerve Schwann cells

TREM-1 mediates interaction between substantia nigra microglia and peripheral neutrophils

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Neural Regeneration Research 2024年第6期19卷 1375-1384页

作者： Tong Shen Guiyun Cui Hao Chen Long Huang Wei Song Jie Zu Wei Zhang Chuanying Xu Liguo Dong Yongmei Zhang jiangsu province key laboratory of Anesthesiology Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina jiangsu province key laboratory of Anesthesia and Analgesia Application Technology Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina NMPA key laboratory for Research and Evaluation of Narcotic and Psychotropic Drugs XuzhouJiangsu ProvinceChina Department of Neurology The Affiliated Hospital of Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina

Microglia-mediated neuroinflammation is considered a pathological feature of Parkinson's *** receptor expressed on myeloid cell-1(TREM-1)can amplify the inherent immune response,and crucially,regulate *** this study,we found marked elevation of serum soluble TREM-1 in patients with Parkinson's disease that positively correlated with Parkinson's disease severity and *** a mouse model of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson's disease,we found that microglial TREM-1 expression also increased in the substantia ***,TREM-1 knockout alleviated dyskinesia in a mouse model of Parkinson's disease and reduced dopaminergic neuronal ***,TREM-1 knockout attenuated the neuroinflammatory response,dopaminergic neuronal injury,and neutrophil ***,we established an in vitro 1-methyl-4-phenyl-pyridine-induced BV2 microglia model of Parkinson's disease and treated the cells with the TREM-1 inhibitory peptide *** found that LP17 treatment reduced apoptosis of dopaminergic neurons and neutrophil ***,inhibition of neutrophil TREM-1 activation diminished dopaminergic neuronal apoptosis induced by ***-1 can activate the downstream CARD9/NF-κB proinflammatory pathway via interaction with *** findings suggest that TREM-1 may play a key role in mediating the damage to dopaminergic neurons in Parkinson's disease by regulating the interaction between microglia and peripheral neutrophils.

关键词： 1-methyl-4-phenylpyridiniumion dopaminergic neurons infiltration 1-methyl-4-phenyl-1 2 3 6-tetrahydropyridine microglia neutrophils neuroinflammation Parkinson's disease SYK TREM-1

Tau truncation in the pathogenesis of Alzheimer's disease:a narrative review

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Neural Regeneration Research 2024年第6期19卷 1221-1232页

作者： Dandan Chu Xingyue Yang Jing Wang Yan Zhou Jin-Hua Gu Jin Miao Feng Wu Fei Liu key laboratory of neuroregeneration of jiangsu and Ministry of Education NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology ProductsCoinnovation Center of NeuroregenerationNantong UniversityNantongJiangsu ProvinceChina Department of Pharmacology School of PharmacyNantong UniversityNantongJiangsu ProvinceChina Department of Biochemistry and Molecular Biology School of MedicineNantong UniversityNantongJiangsu ProvinceChina Department of Clinical Pharmacy Affiliated Maternity and Child Health Care Hospital of Nantong UniversityNantong UniversityNantongJiangsu ProvinceChina laboratory of Animal Center Nantong UniversityNantongJiangsu ProvinceChina Department of Neurochemistry Inge Grundke-Iqbal Research FloorNew York State Institute for Basic Research in Developmental DisabilitiesStaten IslandNYUSA

Alzheimer's disease is characterized by two major neuropathological hallmarks—the extracellularβ-amyloid plaques and intracellular neurofibrillary tangles consisting of aggregated and hyperphosphorylated Tau *** studies suggest that dysregulation of the microtubuleassociated protein Tau,especially specific proteolysis,could be a driving force for Alzheimer's disease *** physiologically promotes the assembly and stabilization of microtubules,whereas specific truncated fragments are sufficient to induce abnormal hyperphosphorylation and aggregate into toxic oligomers,resulting in them gaining prion-like *** addition,Tau truncations cause extensive impairments to neural and glial cell functions and animal cognition and behavior in a fragment-dependent *** review summarizes over 60 proteolytic cleavage sites and their corresponding truncated fragments,investigates the role of specific truncations in physiological and pathological states of Alzheimer's disease,and summarizes the latest applications of strategies targeting Tau fragments in the diagnosis and treatment of Alzheimer's disease.

关键词： Alzheimer's disease cleavage site diagnosis marker neurofibrillary tangles phosphorylation Tau Tau aggregation therapy truncation

Role of CD36 in central nervous system diseases

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Neural Regeneration Research 2024年第3期19卷 512-518页

作者： Min Feng Qiang Zhou Huimin Xie Chang Liu Mengru Zheng Shuyu Zhang Songlin Zhou Jian Zhao School of Health Science and Engineering University of Shanghai for Science and TechnologyShanghaiChina Department of Orthopedic Oncology Second Affiliated Hospital of Naval Medical UniversityShanghaiChina key laboratory of neuroregeneration of jiangsu and Ministry of Education NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology ProductsJiangsu Clinical Medicine Center of Tissue Engineering and Nerve Injury RepairCo-Innovation Center of NeuroregenerationNantong UniversityNantongJiangsu ProvinceChina Department of Stomatology Affiliated Hospital of Nantong UniversityNantongJiangsu ProvinceChina Medical College of Nantong University NantongJiangsu ProvinceChina

CD36 is a highly glycosylated integral membrane protein that belongs to the scavenger receptor class B family and regulates the pathological progress of metabolic ***36 was recently found to be widely expressed in various cell types in the nervous system,including endothelial cells,pericytes,astrocytes,and ***36 mediates a number of regulatory processes,such as endothelial dysfunction,oxidative stress,mitochondrial dysfunction,and inflammatory responses,which are involved in many central nervous system diseases,such as stroke,Alzheimer’s disease,Parkinson’s disease,and spinal cord ***36 antagonists can suppress CD36 expression or prevent CD36 binding to its ligand,thereby achieving inhibition of CD36-mediated pathways or ***,we reviewed the mechanisms of action of CD36 antagonists,such as Salvianolic acid B,tanshinone IIA,curcumin,sulfosuccinimidyl oleate,antioxidants,and small-molecule ***,we predicted the structures of binding sites between CD36 and *** sites can provide targets for more efficient and safer CD36 antagonists for the treatment of central nervous system diseases.

关键词： animal experiments antagonists CD36 antagonist central nervous system diseases clinical trial curcumin microRNA salvianolic acid B small-molecule drugs sulfosuccinimidyl oleate

Dopamine in the prefrontal cortex plays multiple roles in the executive function of patients with Parkinson's disease

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Neural Regeneration Research 2024年第8期19卷 1759-1767页

作者： Zihang Zhou Yalong Yan Heng Gu Ruiao Sun Zihan Liao Ke Xue Chuanxi Tang Department of Neurobiology Xuzhou Key Laboratory of NeurobiologyXuzhou Medical UniversityXuzhouJiangsu ProvinceChina

Parkinson’s disease can affect not only motor functions but also cognitive abilities,leading to cognitive *** common issue in Parkinson’s disease with cognitive dysfunction is the difficulty in executive *** functions help us plan,organize,and control our actions based on our *** brain area responsible for executive functions is called the prefrontal co *** acts as the command center for the brain,especially when it comes to regulating executive *** role of the prefrontal cortex in cognitive processes is influenced by a chemical messenger called ***,little is known about how dopamine affects the cognitive functions of patients with Parkinson’s *** this article,the authors review the latest research on this *** start by looking at how the dopaminergic syste m,is alte red in Parkinson’s disease with executive ***,they explore how these changes in dopamine impact the synaptic structure,electrical activity,and connection components of the prefrontal *** authors also summarize the relationship between Parkinson’s disease and dopamine-related cognitive *** information may offer valuable insights and directions for further research and improvement in the clinical treatment of cognitive impairment in Parkinson’s disease.

关键词： dopamine dopamine receptor dopamine transporter executive dysfunction neural network neural oscillation prefrontal cortex synaptic plasticity

Gut microbiota dysbiosis contributes toα-synuclein-related pathology associated with C/EBPβ/AEP signaling activation in a mouse model of Parkinson’s disease

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Neural Regeneration Research 2024年第9期19卷 2081-2088页

作者： Xiaoli Fang Sha Liu Bilal Muhammad Mingxuan Zheng Xing Ge Yan Xu Shu Kan Yang Zhang Yinghua Yu Kuiyang Zheng Deqin Geng Chun-Feng Liu Department of Neurology and Clinical Research Center of Neurological Disease The Second Affiliated Hospital of Soochow UniversitySuzhouJiangsu ProvinceChina Department of Neurology Affiliated Hospital of Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina jiangsu key laboratory of Immunity and Metabolism Department of Pathogen Biology and ImmunologyXuzhou Medical UniversityXuzhouJiangsu ProvinceChina Department of Neurology Xuzhou Central HospitalXuzhouJiangsu ProvinceChina jiangsu key laboratory of Neuropsychiatric Disease and Institute of Neuroscience Soochow UniversitySuzhouJiangsu ProvinceChina

Parkinson’s disease is a neurodegenerative disease characterized by motor and gastrointestinal *** dysfunction can precede the onset of motor symptoms by several *** microbiota dysbiosis is involved in the pathogenesis of Parkinson’s disease,whether it plays a causal role in motor dysfunction,and the mechanism underlying this potential effect,remain ***/enhancer binding proteinβ/asparagine endopeptidase(C/EBPβ/AEP)signaling,activated by bacterial endotoxin,can promoteα-synuclein transcription,thereby contributing to Parkinson’s disease *** this study,we aimed to investigate the role of the gut microbiota in C/EBPβ/AEP signaling,α-synuclein-related pathology,and motor symptoms using a rotenone-induced mouse model of Parkinson’s disease combined with antibiotic-induced microbiome depletion and fecal microbiota *** found that rotenone administration resulted in gut microbiota dysbiosis and perturbation of the intestinal barrier,as well as activation of the C/EBP/AEP pathway,α-synuclein aggregation,and tyrosine hydroxylase-positive neuron loss in the substantia nigra in mice with motor ***,treatment with rotenone did not have any of these adverse effects in mice whose gut microbiota was depleted by pretreatment with ***,we found that transplanting gut microbiota derived from mice treated with rotenone induced motor deficits,intestinal inflammation,and *** of fecal microbiota from healthy control mice alleviated rotenone-induced motor deficits,intestinal inflammation,endotoxemia,and intestinal barrier *** results highlight the vital role that gut microbiota dysbiosis plays in inducing motor deficits,C/EBPβ/AEP signaling activation,andα-synuclein-related pathology in a rotenone-induced mouse model of Parkinson’s ***,our findings suggest that supplementing with healthy microbiota may be a safe and effective treatment that c

关键词： C/EBP/AEP signaling pathway endotoxemia fecal microbiota transplantation intestinal barrier intestinal inflammation microbiota-gut-brain axis Parkinson’s disease

Anisotropic microtopography surface of chitosan scaffold regulating skin precursor-derived Schwann cells towards repair phenotype promotes neural regeneration

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Regenerative Biomaterials 2024年第3期3卷 68-81页

作者： Meng Cong Xia Wu Lingjie Zhu Guohao Gu Fei Ding Guicai Li Haiyan Shi key laboratory of Neuroregenration of jiangsu and Ministry of Education and Co-Innovation Center of neuroregeneration Nantong UniversityNantong 226001China Department of Pathophysiology School of MedicineNantong UniversityNantong 226001China

For repairing peripheral nerve and spinal cord defects,biomaterial scaffoid-based cell-therapy was emerged as an effective strategy,requiring the positive response of seed cells to biomaterial substrate and environment *** work highlighted that the imposed surface properties of scaffold could provide important guidance cues to adhered cells for ***,the insufficiency of native Schwann cells and unclear cellular response mechanisms remained to be *** that,this study aimed to illuminate the micropatterned chitosan-film action on the rat skin precursor-derived Schwann cells(SKP-SCs).Chitosanfilm with different ridge/groove size was fabricated and applied for the SKP-SCs *** indicated that SKP-SCs cultured on 30μm size microgroove surface showed better oriented alignment *** SKP-sCs presented similar genic phenotype as repair Schwann cells,increasing expression of c-Jun,neural cell adhesion molecule,and neurotrophic receptor ***,SKP-SC-secretome was subjected to cytokine array GS67 assay,data indicated the regulation of paracrine phenotype,a panel of cytokines was verifed up-regulated at secreted level and gene expression level in induced *** up-regulated cytokines exhibit a series of promotive neural regeneration functions,including cell survival,cell migration,cell proliferation,angiogenesis,axon growth,and cellular organization *** bioinformatics ***,the effectively polarized SKP-SCs-sourced secretome,promoted the proliferation and migration capacity of the primarily cultured native rat Schwann cells,and augmented neurites growth of the cultured motoneurons,as well as boosted axonal regrowth of the axotomy-injured *** together,SKP-SCs obtained pro-neuroregeneration phenotype in adaptive response to the anisotropic topography surface of chitosan-film,displayed the oriented parallel growth,the transition towards repair Schwann cell genic phenot

关键词： anisotropic microtopography skin precursor-derived Schwann cells chitosan-flm neural regeneration phenotype regulation