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Enhancing osteogenic bioactivities of coaxial electrospinning nanoscaffolds through incorporating iron oxide nanoparticles and icaritin for bone regeneration

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Nano Research 2024年第7期17卷 6430-6442页

作者： Peng Wang Qianjin Wang Dengxian Wu Yunyang Zhang Shixiong Kang Xucai Wang Jiayu Gu Hao Wu Zhihong Xu Qing Jiang School of Biomedical Engineering and Informatics Nanjing Medical UniversityNanjing 211166China State Key Laboratory of Pharmaceutical Biotechnology Department of Sports Medicine and Adult Reconstructive SurgeryNanjing Drum Tower HospitalThe Affiliated Hospital of Nanjing University Medical SchoolNanjing 210008China center of Modem Analysis Nanjing UniversityNanjing 210008China State Key Laboratory of Bioelectronics Jiangsu Key Laboratory for Biomaterials and DevicesSchool of Biological Science and Medical EngineeringSoutheast UniversityNanjing 210009China Co-Innovation center for Efficient Processing and Utilization of Forest Resources College of Chemical EngineeringNanjing Forestry UniversityNanjing 210037China Jiangsu institute of Metrology Nanjing 210023China

bone tissue engineering provides a promising strategy for the treatment of bone ***,the clinical utilization of biomaterial-based scaffolds is constrained by their inadequate mechanical strength and absence of osteo-inductive ***,we proposed to endow nano-scaffold(NS)constructed by coaxial electrospinning technique with enhanced osteogenic bioactivities and mechanical properties by incorporating biocompatible magnetic iron oxide nanoparticles(IONPs)and icaritin(ICA).Four types of nano-scaffolds(NS,ICA@NS,NS-IONPs and ICA@NS-IONPs)were *** incorporation of ICA and IONPs minimally impact their surface morphological and chemical *** enhanced the mechanical properties of NS scaffolds,including hardness,tensile strength,and elastic *** vitro assessments demonstrated that ICA@NS-IONPs exhibited enhanced osteogenic bioactivities towards mouse calvarial pre-osteoblast cell line MC3T3-E1 as evidenced by detecting the alkaline phosphatase(ALP)activity level,expressions of osteogenesis-related genes and proteins as well as mineralized nodule *** investigations revealed that MEK/ERK(MAP kinase-ERK kinase(MEK)/extracellularsignal-regulated kinase(ERK))signaling pathway could offer a plausible explanation for the osteogenic differentiation of MC3T3-E1 cells induced by ICA@***,the implantation of nano-scaffolds in rat skull defects exhibited a substantial improvement in in vivo bone ***,IONPs and ICA incorporated coaxial electrospinning nano-scaffolds present a novel strategy for the optimization of scaffolds for bone tissue engineering.

关键词： iron oxide nanoparticles icaritin coaxial electrospinning nano-scaffolds MEK/ERK signaling pathway bone regeneration

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Influence on the immune function of the human peripheral blood mononuclear cells transfected by retrovirus-mediated HSV-tk gene

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Chinese Medical Journal 2006年第12期119卷 1038-1041页

作者： XUE Xing-kui SUN Wen-ji HU Jie YAO Hang-ping CAI Zhen bone marrow transplantation center ＆ Department ofHematology First Affiliated Hospital institute of immunology Zhejiang University School of Medicine Hangzhou 310003 China

Graft-versus-host disease （GVHD） is a severe complication and a major source of morbidity and mortality after allogeneic hematopoietic stem cell transplantation （HSCT）. Although T cell depletion of the allogeneic HSCT can efficiently prevent GVHD, it is associated with increased graft rejection and relapse of the malignant disease. To preserve the beneficial effects of donor T cells and avoid their GVHD effects, some approaches have been explored. One of them is to transfer a special suicide gene into the donor T lymphocytes so that they become more sensitive to a specific drug that is ordinarily not toxic. The most commonly used suicide gene is the thymidine kinase-encoding gene of herpes simplex virus （HSV-tk）.

关键词： graft vs host disease genes, transgenic, suicide T-lymphocytes cytotoxicity, immunologic

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IRE1α regulates the PTHrP-IHH feedback loop to orchestrate chondrocyte hypertrophy and cartilage mineralization

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Genes & Diseases 2024年第1期11卷 464-478页

作者： Mengtian Fan Nana Geng Xingyue Li Danyang Yin Yuyou Yang Rong Jiang Cheng Chen Naibo Feng Li Liang Xiaoli Li Fengtao Luo Huabing Qi Qiaoyan Tan Yangli Xie Fengjin Guo Laboratory of Developmental Biology Department of Cell Biology and GeneticsSchool of Basic Medical ScienceChongqing Medical UniversityChongqing 400016China Laboratory of Stem Cells and Tissue Engineering School of Basic Medical ScienceChongqing Medical UniversityChongqing 400016China Department of Orthopedics The 1st Affiliated Hospital of Chongqing Medical UniversityChongqing 400016China Department of Wound Repair and Rehabilitation Medicine State Key Laboratory of TraumaBurns and Combined InjuryTrauma CenterResearch Institute of SurgeryDaping HospitalArmy Medical UniversityChongqing 400042China

Cartilage development is controlled by the highly synergistic proliferation and differentiation of growth plate chondrocytes,in which the Indian hedgehog(IHH)and parathyroid hormone-related protein-parathyroid hormone-1 receptor(PTHrP-PTH1R)feedback loop is *** inositol-requiring enzyme 1a/X-box-binding protein-1 spliced(IRE1α/XBP1s)branch of the unfolded protein response(UPR)is essential for normal cartilage ***,the precise role of ER stress effector IRE1α,encoded by endoplasmic reticulum to nucleus signaling 1(ERN1),in skeletal development remains ***,we reported that loss of IRE1α accelerates chondrocyte hypertrophy and promotes endochondral bone ***1 acts as a negative regulator of chondrocyte proliferation and differentiation in postnatal growth *** deficiency interrupted PTHrP/PTH1R and IHH homeostasis leading to impaired chondrocyte hypertrophy and ***1s,produced by p-IRE1α-mediated splicing,binds and up-regulates PTH1R and IHH,which coordinate cartilage ***,ER stress cannot be activated normally in ERN1-deficient *** conclusion,ERN1 deficiency accelerates chondrocyte hypertrophy and cartilage mineralization by impairing the homeostasis of the IHH and PTHrP/PTH1R feedback loop and ER ***1 may have a potential role as a new target for cartilage growth and maturation.

关键词： Cartilage development ER stress ERN1 IHH PTHrP/PTH1R

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Human CD39hi regulatory T cells present stronger stability and function under inflammatory conditions

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Cellular & Molecular immunology 2017年第6期14卷 521-528页

作者： Jian Gu Xuhao Ni Xiongxiong Pan Hao Lu Yunjie Lu Jie Zhao Song Guo Zheng Keli L Hippen Xuehao Wang Ling Lu Translational Medicine Research center Affiliated Jiangning Hospital and Liver Transplantation Center First Affiliated Hospital Nanjing Medical University Nanjing 210029 China University of Minnesota Cancer center and Division of bone marrow transplantation Department of Pediatrics University of Minnesota Minneapolis MN 55455 USA Division of Rheumatology Penn State Milton S. Hershey Medical Center Hershey PA 17033 USA

Autoimmune diseases are characterized by an imbalance between regulatory T cells and effector T-cell subsets, such as Thl and Th17 cells. Studies have confirmed that natural CD4＋Foxp3＋ Tregs were unstable and dysfunctional in the presence of pro-inflammatory cytokines. In the current study, human CD39hi Tregs and CD39low Tregs were sorted from Tregs in vitro after 7 days of expansion. The functions of both Treg subsets were investigated under inflammatory conditions in vitro and in vivo. In the presence of IL-1β and IL-6, cultured CD4＋CD39hi Tregs maintained stable forkhead box protein 3 expression, whereas CD4＋CD39low Tregs lost Foxp3 expression and trans-differentiated into Thl or Th17 cells. Decreased IL-1βR and IL-6R expression on the CD39hi Tregs was the primary mechanism responsible for Treg stability. In addition, reduced activation of downstream molecules, such as STAT1 and STAT3, through the modulation of CpG demethylation played an important role. Finally, human CD4＋CD39hi Tregs but not CD4＋CD39low Tregs protected against xenograft versus host disease in model mice. These results strongly implied the physiological importance of CD39 expression and suggested that manipulation of CD39hi Tregs might represent a novel strategy for the treatment of autoimmune diseases.

关键词： CD39 stability Tregs xeno-GVHD

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机械敏感蛋白PC1调控破骨细胞及骨吸收的作用机制

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Science Bulletin 2024年第12期69卷 1964-1979页

作者：黄梅周静璇李潇骁刘冉姜洋子陈开璇焦玉睿尹欣刘玲孙宇晨王维山肖业苏甜郭奇黄燕杨觅魏婕 L.Darryl Quarles 肖洲生曾超罗湘杭雷光华李长俊 Department of Endocrinology Endocrinology Research CenterXiangya HospitalCentral South UniversityChangsha 410008China Hunan Key Laboratory of Joint Degeneration and Injury Changsha 410008China Key Laboratory of Aging-related bone and Joint Diseases Prevention and Treatment Ministry of EducationXiangya HospitalCentral South UniversityChangsha 410008China School of Biomedical Sciences Institute for Tissue Engineering and Regenerative MedicineFaculty of MedicineThe Chinese University of Hong KongHong Kong 999077China Key Laboratory for Regenerative Medicine Ministry of EducationSchool of Biomedical SciencesFaculty of MedicineThe Chinese University of Hong KongHong Kong 999077China center for Neuromusculoskeletal Restorative Medicine(CNRM) The Chinese University of Hong KongHong Kong 999077China Department of Orthopaedics The First Affiliated Hospital of Shihezi UniversityShihezi 832061China Department of Orthopaedics Xiangya HospitalCentral South UniversityChangsha 410008China Department of Epidemiology and Health Statistics Xiangya School of Public HealthCentral South UniversityChangsha 410008China Department of Medicine University of Tennessee Health Science CenterMemphis 38163USA National Clinical Research center for Geriatric Disorders Xiangya HospitalCentral South UniversityChangsha 410008China Laboratory Animal center Xiangya HospitalCentral South UniversityChangsha 410008China

Mechanical loading is required for bone homeostasis,but the underlying mechanism is still *** previous studies revealed that the mechanical protein polycystin-1(PC1,encoded by Pkd1)is critical for bone ***,the role of PC1 in bone resorption is ***,we found that PC1directly regulates osteoclastogenesis and bone *** conditional deletion of Pkd1 in the osteoclast lineage resulted in a reduced number of osteoclasts,decreased bone resorption,and increased bone mass.A cohort study of 32,500 patients further revealed that autosomal dominant polycystic kidney disease,which is mainly caused by loss-of-function mutation of the PKD1 gene,is associated with a lower risk of hip fracture than those with other chronic kidney ***,mice with osteoclastspecific knockout of Pkd1 showed complete resistance to unloading-induced bone loss.A mechanistic study revealed that PC1 facilitated TAZ nuclear translocation via the C-terminal tail-TAZ complex and that conditional deletion of Taz in the osteoclast lineage resulted in reduced osteoclastogenesis and increased bone *** regulation of the PC1-TAZ axis alleviated unloading-and estrogen deficiency-induced bone ***,the PC1-TAZ axis may be a potential therapeutic target for osteoclast-related osteoporosis.

关键词： Polycystin1 Osteoclastogenesis bone resorption Mechanical stress

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Transcriptional regulation of the immune checkpoints PD-1 and CTLA-4

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Cellular & Molecular immunology 2022年第7期19卷 861-862页

作者： Jing Guo Zhonghui Xue Lie Wang institute of immunology and bone marrow transplantation center The First Affiliated HospitalZhejiang University School of MedicineHangzhouZhejiang310006China Department of Microbiology and immunology Stanford University School of MedicineStanfordCA94305USA Research center of Clinical Medicine Affiliated Hospital of Nantong UniversityNantongJiangsu226001China Liangzhu Laboratory Zhejiang University Medical CenterHangzhouZhejiang311121China

Immunotherapy targeting immune checkpoints(ICs)has revolutionized the field of cancer *** are a group of proteins that provide stimulatory or inhibitory signals to regulate T-cell activation,tolerance,and *** date,some immune checkpoint inhibitors(ICIs)targeting TIM-3,LAG-3,TIGIT,and VISTA are under investigation for their clinical ***,only ICIs against CTLA-4,PD-1,and PD-L1 are approved by the FDA and widely used as first-line or second-line treatments for multiple cancer ***-4 and PD-1 are coinhibitory receptors that are mainly expressed by T cells.

关键词： immune cancer clinical

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Multi-omics analysis of human tendon adhesion reveals that ACKR1-regulated macrophage migration is involved in regeneration

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bone Research 2024年第2期12卷 390-406页

作者： Xinshu Zhang Yao Xiao Bo Hu Yanhao Li Shaoyang Zhang Jian Tian Shuo Wang Zaijin Tao Xinqi Zeng Ning-Ning Liu Baojie Li Shen Liu Department of Orthopaedics Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University School of Medicine600 Yishan RdShanghai 200233PR China Section of Spine Surgery Department of OrthopaedicsChangzheng HospitalNaval Medical UniversityShanghai 200003PR China Bio-X institutes Key Laboratory for the Genetics of Developmental and Neuropsychiatric DisordersMinistry of EducationShanghai Jiao Tong UniversityShanghai 200241PR China Department of Orthopaedics Wuxi Ninth People’s Hospital Affiliated to Soochow UniversityWuxi 214062PR China State Key Laboratory of Systems Medicine for Cancer Center for Single-Cell OmicsSchool of Public HealthShanghai Jiao Tong University School of MedicineShanghai 200025China

Tendon adhesion is a common complication after tendon injury with the development of accumulated fibrotic tissues without effective anti-fibrotic therapies,resulting in severe *** are widely recognized as a fibrotic trigger during peritendinous adhesion ***,different clusters of macrophages have various functions and receive multiple regulation,which are both still *** our current study,multi-omics analysis including single-cell RNA sequencing and proteomics was performed on both human and mouse tendon adhesion tissue at different stages after tendon *** transcriptomes of over 74000 human single cells were *** results,we found that SPP1^(+)macrophages,RGCC^(+)endothelial cells,ACKR1^(+)endothelial cells and ADAM12^(+)fibroblasts participated in tendon adhesion ***,despite specific fibrotic clusters in tendon adhesion,FOLR2^(+)macrophages were identified as an antifibrotic cluster by in vitro experiments using human ***,ACKR1 was verified to regulate FOLR2^(+)macrophages migration at the injured peritendinous site by transplantation of bone marrow from Lysm-Cre;R26R^(tdTomato) mice to lethally irradiated Ackr1^(-/-)mice(Ackr1^(-/-)chimeras;deficient in ACKR1)and control mice(WT chimeras).Compared with WT chimeras,the decline of FOLR2^(+)macrophages was also observed,indicating that ACKR1 was specifically involved in FOLR2^(+)macrophages *** together,our study not only characterized the fibrosis microenvironment landscape of tendon adhesion by multi-omics analysis,but also uncovered a novel antifibrotic cluster of macrophages and their *** results provide potential therapeutic targets against human tendon adhesion.

关键词： tendon analysis landscape

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Inflammation and aging:signaling pathways and intervention therapies

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Signal Transduction and Targeted Therapy 2023年第7期8卷 3267-3295页

作者： Xia Li Chentao Li Wanying Zhang Yanan Wang Pengxu Qian He Huang bone marrow transplantation center the First Affiliated HospitalZhejiang University School of MedicineHangzhouPeople’s Republic of China Liangzhu Laboratory Zhejiang University Medical Center1369 West Wenyi RoadHangzhou 311121China institute of Hematology Zhejiang University&Zhejiang Engineering Laboratory for Stem Cell and ImmunotherapyHangzhou 310058China Zhejiang Province Engineering Laboratory for Stem Cell and Immunity Therapy Hangzhou 310058China Zhejiang UniversityUniversity of Edinburgh institute Zhejiang University School of MedicineZhejiang UniversityHainingChina center for Stem Cell and Regenerative Medicine and bone marrow transplantation center of the first affiliated hospital Zhejiang University School of MedicineHangzhou 310058China

Aging is characterized by systemic chronic inflammation,which is accompanied by cellular senescence,immunosenescence,organ dysfunction,and age-related *** the multidimensional complexity of aging,there is an urgent ne... 详细信息

关键词： aging reduction dimensionality

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Tumor extracellular vesicles mediate anti-PD-L1 therapyresistance by decoying anti-PD-L1

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Cellular & Molecular immunology 2022年第11期19卷 1290-1301页

作者： Jiming Chen Jie Yang Wenhui Wang Danfeng Guo Chengyan Zhang Shibo Wang Xinliang Lu Xiaofang Huang Pingli Wang Gensheng Zhang Jing Zhang Jianli Wang Zhijian Cai institute of immunology and Department of Orthopaedics of the Second Affiliated HospitalZhejiang University School of Medicine310058 HangzhouChina Henan Key Laboratory for Digestive Organ transplantation The First Affiliated Hospital of Zhengzhou University450052 ZhengzhouChina Department of Critical Care Medicine Qilu HospitalCheeloo College of MedicineShandong University250063 JinanChina Department of Respiratory and Critical Care Medicine The Second Affiliated Hospital of Zhejiang University School of Medicine310003 HangzhouChina Department of Critical Care Medicine of the Second affiliated hospital Zhejiang University School of Medicine310003 HangzhouChina Department of Pathology Zhejiang University First Affiliated Hospital and School of Medicine310002 HangzhouChina institute of immunology and Bone Marrow Transplantation Center of the First Affiliated HospitalZhejiang University School of Medicine310058 HangzhouChina institute of Hematology Zhejiang University&Zhejiang Engineering Laboratory for Stem Cell and Immunotherapy310006 HangzhouChina

PD-L1+tumor-derived extracellular vesicles(TEVs)cause systemic immunosuppression and possibly resistance to anti-PD-L1 antibody(αPD-L1)***,whether and how PD-L1+TEVs mediateαPD-L1 therapy resistance is ***,we show that PD-L1+TEVs substantially decoyαPD-L1 and that TEV-boundαPD-L1 is more rapidly cleared by macrophages,causing insufficient blockade of tumor PD-L1 and subsequentαPD-L1 therapy *** of endogenous production of TEVs by Rab27a or Coro1a knockout reversesαPD-L1 therapy *** an increasedαPD-L1 dose or macrophage depletion mediated by the clinical drug pexidartinib abolishesαPD-L1 therapy ***,in the treatment cycle with the same total treatment dose ofαPD-L1,high-dose and low-frequency treatment had better antitumor effects than low-dose and highfrequency treatment,induced stronger antitumor immune memory,and eliminatedαPD-L1 therapy ***,in humanized immune system mice with human xenograft tumors,both increasedαPD-L1 dose and high-dose and low-frequency treatment enhanced the antitumor effects ofα***,increased doses ofαPD-L1 andαPD-1 had comparable antitumor effects,butαPD-L1 amplified fewer PD-1+Treg cells,which are responsible for tumor ***,our results reveal a TEV-mediated mechanism ofαPD-L1-specific therapy resistance,thus providing promising strategies to improveαPD-L1 efficacy.

关键词： Tumor Extracellular vesicles PD-L1

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Targeted knockdown of PGAM5 in synovial macrophages efficiently alleviates osteoarthritis

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bone Research 2024年第1期12卷 215-226页

作者： Yuhang Liu Ruihan Hao Jia Lv Jie Yuan Xuelei Wang Churong Xu Ding Ma Zhouyi Duan Bingjun Zhang Liming Dai Yiyun Cheng Wei Lu Xiaoling Zhang Department of Orthopedic Surgery Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine(SJTUSM)Shanghai 200092China National Facility for Translational Medicine Shanghai 200240China Shanghai Frontiers Science center of Genome Editing and Cell Therapy Shanghai Key Laboratory of Regulatory BiologySchool of Life SciencesEast China Normal UniversityShanghai 200241China Department of Orthopaedic Surgery The Second Hospital of Shanxi Medical UniversityTaiyuan 030001China CAS Key Laboratory of Tissue Microenvironment and Tumor Shanghai Institute of Nutrition and HealthChinese Academy of SciencesShanghai 200031China School of Medicine Shanghai UniversityShanghai 200444China

Osteoarthritis(OA)is a common degenerative disease worldwide and new therapeutics that target inflammation and the crosstalk between immunocytes and chondrocytes are being developed to prevent and treat *** attempts involve repolarizing pro-inflammatory M1 macrophages into the anti-inflammatory M2 phenotype in *** this study,we found that phosphoglycerate mutase 5(PGAM5)significantly increased in macrophages in OA synovium compared to controls based on histology of human samples and single-cell RNA sequencing results of mice *** address the role of PGAM5 in macrophages in OA,we found conditional knockout of PGAM5 in macrophages greatly alleviated OA symptoms and promoted anabolic metabolism of chondrocytes in vitro and in ***,we found that PGAM5 enhanced M1 polarization via AKT-mTOR/p38/ERK pathways,whereas inhibited M2 polarization via STAT6-PPARγpathway in murine bone marrow-derived ***,we found that PGAM5 directly dephosphorylated Dishevelled Segment Polarity Protein 2(DVL2)which resulted in the inhibition ofβ-catenin and repolarization of M2 macrophages into M1 *** knockout of both PGAM5 andβ-catenin in macrophages significantly exacerbated osteoarthritis compared to PGAM5-deficient *** by these findings,we successfully designed mannose modified fluoropolymers combined with siPGAM5 to inhibit PGAM5 specifically in synovial macrophages via intra-articular injection,which possessed desired targeting abilities of synovial macrophages and greatly attenuated murine ***,these findings defined a key role for PGAM5 in orchestrating macrophage polarization and provides insights into novel macrophage-targeted strategy for treating OA.

关键词： osteoarthritis metabolism inhibited

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