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Dendritic shrinkage after injury: a cellular killer or a necessity for axonal regeneration?

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Neural regeneration research 2019年第8期14卷 1313-1316页

作者： An Beckers Lieve Moons Neural Circuit development and regeneration research Group Department of BiologyKU Leuven

Dendrites form an essential component of the neuronal circuit have been largely overlooked in regenerative research. Nevertheless, subtle changes in the dendritic arbors of neurons are one of the first stages of various neurodegenerative diseases, leading to dysfunctional neuronal networks and ultimately cellular death. Maintaining dendrites is therefore considered an essential neuroprotective strategy. This mini-review aims to discuss an intriguing hypothesis, which postulates that dendritic shrinkage is an important stimulant to boost axonal regeneration, and thus that preserving dendrites might not be the ideal therapeutic method to regain a full functional network upon central nervous system damage. Indeed, our study in zebrafish, a versatile animal model with robust regenerative capacity recently unraveled that dendritic retraction is evoked prior to axonal regrowth after optic nerve injury. Strikingly, inhibiting dendritic pruning upon damage perturbed axonal regeneration. This constraining effect of dendrites on axonal regrowth has sporadically been proposed in literature, as summarized in this short narrative. In addition, the review discusses a plausible underlying mechanism for the observed antagonistic axon-dendrite interplay, which is based on energy restriction inside neurons. Axonal injury indeed leads to a high local energy demand in which efficient axonal energy supply is fundamental to ensure regrowth. At the same time, axonal lesion is known to induce m让ochondrial depolarization, causing energy depletion in the axonal compartment of damaged neurons. Mitochondria, however, become mostly stationary after development, which has been proposed as a potential underlying reason for the low regenerative capacity of adult mammals. Per contra, upon reduced neuronal activity, mitochondrial mobility enhances. In this view, dendritic shrinkage after axonal injury in zebrafish could result in less synaptic input and hence, a release of mitochondria within the soma-dendrite compartment that then translocate to

关键词： axonal regeneration dendritic remodeling retina central nervous system zebrafish mitochondrial transport mitochondrial dynamics energy supply

Overview of the main biological mechanisms linked to changes in periodontal ligament stem cells and the inflammatory microenvironment

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2023年第5期24卷 373-386页

作者： Xuetao ZHAO Hongbing LIN Tong DING Yawei WANG Na LIU Yuqin SHEN Department of Periodontics Jilin Provincial Key Laboratory of Tooth Development and Bone RemodelingHospital of StomatologyJilin UniversityChangchun 130021China Department of Periodontics Affiliated Stomatology Hospital of Guangzhou Medical UniversityGuangzhou Key Laboratory of Basic and Applied Research of Oral Regenerative MedicineGuangzhou 510182China

Periodontitis is a complex chronic inflammatory disease.The invasion of pathogens induces the inflammatory microenvironment in periodontitis.Cell behavior changes in response to changes in the microenvironment,which in turn alters the local inflammatory microenvironment of the periodontium through factors secreted by cells.It has been confirmed that periodontal ligament stem cells(PDLSCs)are vital in the development of periodontal disease.Moreover,PDLSCs are the most effective cell type to be used for periodontium regeneration.This review focuses on changes in PDLSCs,their basic biological behavior,osteogenic differentiation,and drug effects caused by the inflammatory microenvironment,to provide a better understanding of the influence of these factors on periodontal tissue homeostasis.In addition,we discuss the underlying mechanism in detail behind the reciprocal responses of PDLSCs that affect the microenvironment.

关键词： Inflammatory microenvironment Inflammatory regulation Osteogenic differentiation Periodontal ligament stem cells Periodontitis

Chitin-glucan improves important pathophysiological features of irritable bowel syndrome

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World Journal of Gastroenterology 2024年第16期30卷 2258-2271页

作者： Caroline Valibouze Caroline Dubuquoy Philippe Chavatte Michaël Genin Veronique Maquet Salvatore Modica Pierre Desreumaux Christel Rousseaux Department of Digestive Surgery and Transplantation Lille UniversityLille 59037France Intestinal Biotech development Facultéde MédicineLille 59045France U1286-INFINITE-Institute for Translational research in Inflammation Universitéde LilleLille 59000France ULR 2694-METRICS Évaluation des Technologies de santéet des Pratiques MédicalesUniversity of LilleLille 59000France KitoZyme SA Institution SociétéAnonymeZone 2Parc des Hauts SartsRue de MilmortHerstal 4040Belgium Hepato-Gastroenterology Department Lille University HospitalLille 59037France

BACKGROUND Irritable bowel syndrome(IBS)is one of the most frequent and debilitating conditions leading to gastroenterological referrals.However,recommended treatments remain limited,yielding only limited therapeutic gains.Chitin-glucan(CG)is a novel dietary prebiotic classically used in humans at a dosage of 1.5-3.0 g/d and is considered a safe food ingredient by the European Food Safety Authority.To provide an alternative approach to managing patients with IBS,we performed preclinical molecular,cellular,and animal studies to evaluate the role of chitin-glucan in the main pathophysiological mechanisms involved in IBS.AIM To evaluate the roles of CG in visceral analgesia,intestinal inflammation,barrier function,and to develop computational molecular models.METHODS Visceral pain was recorded through colorectal distension(CRD)in a model of long-lasting colon hypersensitivity induced by an intra-rectal administration of TNBS[15 milligrams(mg)/kilogram(kg)]in 33 Sprague-Dawley rats.Intracolonic pressure was regularly assessed during the 9 wk-experiment(weeks 0,3,5,and 7)in animals receiving CG(n=14)at a human equivalent dose(HED)of 1.5 g/d or 3.0 g/d and compared to negative control(tap water,n=11)and positive control(phloroglucinol at 1.5 g/d HED,n=8)groups.The anti-inflammatory effect of CG was evaluated using clinical and histological scores in 30 C57bl6 male mice with colitis induced by dextran sodium sulfate(DSS)administered in their drinking water during 14 d.HT-29 cells under basal conditions and after stimulation with lipopolysaccharide(LPS)were treated with CG to evaluate changes in pathways related to analgesia μ-opioid receptor(MOR),cannabinoid receptor 2(CB2),peroxisome proliferator-activated receptor alpha,inflammation[interleukin(IL)-10,IL-1b,and IL-8]and barrier function[mucin 2-5AC,claudin-2,zonula occludens(ZO)-1,ZO-2]using the real-time PCR method.Molecular modelling of CG,LPS,lipoteichoic acid(LTA),and phospholipomannan(PLM)was developed,and the ability of CG to chelate microbial pathogenic lipids

关键词： Chitin-glucan Irritable bowel syndrome Abdominal pain Inflammation Intestinal barrier Molecular modelling Microbial cell walls chelation

Aging-induced memory loss due to decreased N1-acetyl-5-methoxykynuramine, a melatonin metabolite, in the hippocampus:a potential prophylactic agent for dementia

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Neural regeneration research 2025年第6期 1705-1706页

作者： Kazuki Watanabe Atsuhiko Hattori Department of Immunobiology Institute of Development Aging and Cancer Tohoku University Department of Sport and Wellness College of Sport and Wellness Rikkyo University

Melatonin (N-acetyl-5-methoxytryptamine) is known as the hormone of darkness because it is synthesized at night and involved in regulating the circadian clock.The hormone is primarily synthesized by the vertebrate pineal gland,but is ubiquitous among invertebrates,unicellular organisms,plants,and even cyanobacteria (Hattori and Suzuki,2024).Melatonin is well-conserved evolutionarily and possesses several physiological functions,such as immune response,bone and glucose metabolism,and memory formation besides regulating the circadian rhythm.

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Harnessing innate immune pathways for therapeutic advancement in cancer

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Signal Transduction and Targeted Therapy 2024年第4期9卷 1506-1564页

作者： Ankang Hu Li Sun Hao Lin Yuheng Liao Hui Yang Ying Mao Department of Neurosurgery Huashan HospitalFudan UniversityShanghaiP.R.China Institute for Translational Brain research Shanghai Medical CollegeFudan University ShanghaiPR.China National Center for Neurological Disorders Huashan HospitalShanghai Medical CollegeFudan UniversityShanghaiP.R.China Shanghai Key Laboratory of Brain Function Restoration and Neural regeneration Shanghai Clinical Medical Center of NeurosurgeryNeurosurgical Institute of Fudan UniversityHuashan HospitalShanghai Medical CollegeFudan UniversityShanghaiP.R.China State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science and MOE Frontiers Center for Brain Science Institutes of Brain ScienceShanghai Medical CollegeFudan UniversityShanghaiP.R.China Shanghai Key Laboratory of Medical Epigenetics International Co-laboratory of Medical Epigenetics and Metabolism(Ministry of Science and Technology)and Key Laboratory of Metabolism and Molecular Medicine(Ministry of Education)and Molecular and Cell Biology LabInstitutes of Biomedical SciencesShanghai Medical College of Fudan UniversityShanghaiP.R.China

The innate immune pathway is receiving increasing attention in cancer therapy.This pathway is ubiquitous across various cell types,not only in innate immune cells but also in adaptive immune cells,tumor cells,and stromal cells.Agonists targeting the innate immune pathway have shown profound changes in the tumor microenvironment(TME)and improved tumor prognosis in preclinical studies.However,to date,the clinical success of drugs targeting the innate immune pathway remains limited.Interestingly,recent studies have shown that activation of the innate immune pathway can paradoxically promote tumor progression.The uncertainty surrounding the therapeutic effectiveness of targeted drugs for the innate immune pathway is a critical issue that needs immediate investigation.In this review,we observe that the role of the innate immune pathway demonstrates heterogeneity,linked to the tumor development stage,pathway status,and specific cell types.We propose that within the TME,the innate immune pathway exhibits multidimensional diversity.This diversity is fundamentally rooted in cellular heterogeneity and is manifested as a variety of signaling networks.The pro-tumor effect of innate immune pathway activation essentially reflects the suppression of classical pathways and the activation of potential pro-tumor alternative pathways.Refining our understanding of the tumor's innate immune pathway network and employing appropriate targeting strategies can enhance our ability to harness the anti-tumor potential of the innate immune pathway and ultimately bridge the gap from preclinical to clinicalapplication.

关键词： drugs therapeutic innate

New pathogenic insights from large animal models of neurodegenerative diseases

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Protein & Cell 2022年第10期13卷 707-720页

作者： Peng Yin Shihua Li Xiao-Jiang Li Weili Yang Guangdong Key Laboratory of Non-human Primate research Guangdong-Hongkong-Macao Institute of CNS RegenerationJinan UniversityGuangzhou 510632China

Animal models are essential for investigating the pathogenesis and developing the treatment of human diseases.Identification of genetic mutations responsible for neurodegenerative diseases has enabled the creation of a large number of small animal models that mimic genetic defects found in the affected individuals.Of the current animal models,rodents with genetic modifications are the most commonly used animal models and provided important insights into pathogenesis.However,most of genetically modified rodent models lack overt neurodegeneration,imposing challenges and obstacles in utilizing them to rigorously test the therapeutic effects on neurodegeneration.Recent studies that used CRISPR/Cas9-targeted large animal(pigs and monkeys)have uncovered important pathological events that resemble neurodegeneration in the patient’s brain but could not be produced in small animal models.Here we highlight the unique nature of large animals to model neurodegenerative diseases as well as the limitations and challenges in establishing large animal models of neurodegenerative diseases,with focus on Huntington disease,Amyotrophic lateral sclerosis,and Parkinson diseases.We also discuss how to use the important pathogenic insights from large animal models to make rodent models more capable of recapitulating important pathological features of neurodegenerative diseases.

关键词： large animal models neurodegenerative diseases CRISPR/Cas9

CRISPR-Based Genome-Editing Tools for Huntington’s Disease research and Therapy

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Neuroscience Bulletin 2022年第11期38卷 1397-1408页

作者： Yiyang Qin Shihua Li Xiao-Jiang Li Su Yang Guangdong Key Laboratory of Non-human Primate research Guangdong-Hongkong-Macao Institute of CNS RegenerationJinan UniversityGuangzhou 510632China

Huntington’s disease(HD)is an autosomal dominantly-inherited neurodegenerative disease,which is caused by CAG trinucleotide expansion in exon 1 of the Huntingtin(HTT)gene.Although HD is a rare disease,its monogenic nature makes it an ideal model in which to understand pathogenic mechanisms and to develop therapeutic strategies for neurodegenerative diseases.Clustered regularly-interspaced short palindromic repeats(CRISPR)is the latest technology for genome editing.Being simple to use and highly efficient,CRISPR-based genome-editing tools are rapidly gaining popularity in biomedical research and opening up new avenues for disease treatment.Here,we review the development of CRISPR-based genome-editing tools and their applications in HD research to offer a translational perspective on advancing the genome-editing technology to HD treatment.

关键词： Huntington’s disease CRISPR Animal models

Highly Aligned Ternary Nanofiber Matrices Loaded with MXene Expedite regeneration of Volumetric Muscle Loss

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Nano-Micro Letters 2024年第4期16卷 269-292页

作者： Moon Sung Kang Yeuni Yu Rowoon Park Hye Jin Heo Seok Hyun Lee Suck Won Hong Yun Hak Kim Dong‑Wook Han Department of Cogno‑Mechatronics Engineering College of Nanoscience and NanotechnologyPusan National UniversityBusan 46241Republic of Korea Medical research Institute School of MedicinePusan National UniversityYangsan 50612Republic of Korea Department of Anatomy School of MedicinePusan National UniversityYangsan 50612Republic of Korea Engineering research Center for Color‑Modulated Extra‑Sensory Perception Technology Pusan National UniversityBusan 46241Republic of Korea Department of Biomedical Informatics School of MedicinePusan National UniversityYangsan 50612Republic of Korea Periodontal Disease Signaling Network research Center and Dental and Life Science Institute School of DentistryPusan National UniversityYangsan 50612Republic of Korea BIO‑IT Fusion Technology research Institute Pusan National UniversityBusan 46241Republic of Korea Present Address:Osstem Implant Inc. Seoul 07789Republic of Korea

Current therapeutic approaches for volumetric muscle loss(VML)face challenges due to limited graft availability and insufficient bioactivities.To overcome these limitations,tissue-engineered scaffolds have emerged as a promising alternative.In this study,we developed aligned ternary nanofibrous matrices comprised of poly(lactide-co-ε-caprolactone)integrated with collagen and Ti_(3)C_(2)T_(x)MXene nanoparticles(NPs)(PCM matrices),and explored their myogenic potential for skeletal muscle tissue regeneration.The PCM matrices demonstrated favorable physicochemical properties,including structural uniformity,alignment,microporosity,and hydrophilicity.In vitro assays revealed that the PCM matrices promoted cellular behaviors and myogenic differentiation of C2C12 myoblasts.Moreover,in vivo experiments demonstrated enhanced muscle remodeling and recovery in mice treated with PCM matrices following VML injury.Mechanistic insights from next-generation sequencing revealed that MXene NPs facilitated protein and ion availability within PCM matrices,leading to elevated intracellular Ca^(2+)levels in myoblasts through the activation of inducible nitric oxide synthase(i NOS)and serum/glucocorticoid regulated kinase 1(SGK1),ultimately promoting myogenic differentiation via the m TOR-AKT pathway.Additionally,upregulated i NOS and increased NO–contributed to myoblast proliferation and fiber fusion,thereby facilitating overall myoblast maturation.These findings underscore the potential of MXene NPs loaded within highly aligned matrices as therapeutic agents to promote skeletal muscle tissue recovery.

关键词： Ti_(3)C_(2)T_(x)MXene nanoparticle Ternary nanofibrous matrices Myogenesis regeneration of volumetric muscle loss Next generation sequencing

Small molecules facilitate single factor-mediated sweat gland cell reprogramming

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Military Medical research 2022年第6期9卷 655-667页

作者： Shuai-Fei Ji Lai-Xian Zhou Zhi-Feng Sun Jiang-Bing Xiang Shao-Yuan Cui Yan Li Hua-Ting Chen Yi-Qiong Liu Huan-Huan Gao Xiao-Bing Fu Xiao-Yan Sun research Center for Tissue Repair and regeneration Affiliated To Medical Innovation research Department and 4th Medical Center PLA General Hospital and PLA Medical CollegePLAKey Laboratory of Tissue Repairand Regenerative Medicine and BeijingKey Research Laboratoryof Skin InjuryRepair and Regeneration28 FuXing RoadBeijing 100853China research unit of Trauma Care Tissue Repair and RegenerationChinese Academy of Medical Sciences2019RU051Beijing 100048China Departmentof Respiratory the Second Medical CenterChinese PLA General HospitalBeijing 100036China Bioengineering College of Chongqing University Chongqing 400044China Department of Nephrology the First Medical CenterChinese PLA General HospitalState Key Laboratory of Kidney DiseasesBeijing 100048China

Background: Large skin defects severely disrupt the overall skin structure and can irreversibly damage sweat glands(SGs), thus impairing the skin’s physiological function. This study aims to develop a stepwise reprogramming strategy to convert fibroblasts into SG lineages, which may provide a promising method to obtain desirable cell types for the functional repair and regeneration of damaged skin.Methods: The expression of the SG markers cytokeratin 5(CK5), cytokeratin 10(CK10), cytokeratin 18(CK18), carcinoembryonic antigen(CEA), aquaporin 5(AQP5) and α-smooth muscle actin(α-SMA) was assessed with quantitative PCR(qPCR), immunofluorescence and flow cytometry. Calcium activity analysis was conducted to test the function of induced SG-like cells(iSGCs). Mouse xenograft models were also used to evaluate the in vivo regeneration of iSGCs.BALB/c nude mice were randomly divided into normal group, SGM treatment group and iSGC transplantation group.Immunocytochemical analyses and starch-iodine sweat tests were used to confirm the in vivo regeneration of iSGCs.Results: Ectodermal dysplasia antigen(EDA) overexpression drove human dermal fibroblast(HDF) conversion into i SGCs in SG culture medium(SGM). qPCR indicated significantly increased mRNA levels of the SG markers CK5, CK18and CEA in iSGCs, and flow cytometry data demonstrated(4.18±0.04)% of iSGCs were CK5 positive and(4.36±0.25)%of iSGCs were CK18 positive. The addition of chemical cocktails greatly accelerated the SG fate program. qPCR results revealed significantly increased mRNA expression of CK5, CK18 and CEA in iSGCs, as well as activation of the duct marker CK10 and luminal functional marker AQP5. Flow cytometry indicated, after the treatment of chemical cocktails,(23.05±2.49)% of iSGCs expressed CK5^(+) and(55.79±3.18)% of iSGCs expressed CK18^(+), respectively. Calcium activity analysis indicated that the reactivity of iSGCs to acetylcholine was close to that of primary SG cells [(60.79±7.71)% vs.(70.59±0.34)%, ns]. In vivo transplantation experiments showe

关键词： Direct reprogramming Human dermal fibroblasts Sweat gland regeneration