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Bioactive Materials 2022年第2期7卷 559-572页

作者： Shue Jin Jing Gao Renli Yang Chen Yuan Ruili Wang Qin Zou Yi Zuo Meifang Zhu Yubao Li Yi Man Jidong Li Research Center for Nano-Biomaterials Analytical and Testing CenterSichuan UniversityChengdu610064PR China State Key Laboratory of Oral Diseases West China Hospital of StomatologySichuan UniversityChengdu610065PR China State Key Laboratory for Modification of Chemical Fibers and Polymer Materials College of Materials Science and EngineeringDonghua UniversityShanghai201620PR China

We demonstrate a simple,effective and feasible method to address the shrinkage of Poly(lactic-co-glycolic acid)(PLGA)through a core-shell structure fiber strategy.The results revealed that introducing size-stable poly-caprolactone(PCL)as the core fiber significantly improved the PLGA-based fibrous scaffold’s dimensional maintenance.We further utilized fish collagen to modify the PLGA shell layer(PFC)of coaxial fibers and loaded baicalin(BA)into the PCL core layer(PCL-BA)to endow fibrous scaffold with more functional biological cues.The PFC/PCL-BA fibrous scaffold promoted the osteogenic differentiation of bone mesenchymal stem cells and stimulated the RAW264.7 cells to polarize into a pro-reparative phenotype.Importantly,the in vivo study demonstrated that the PFC/PCL-BA scaffold could regulate inflammation and osteoclast differentiation,favor neovascularization and bone formation.This work tactfully combined PLGA and PCL to establish a drug release platform based on the core-shell fibrous scaffold for vascularized bone regeneration.

关键词： Coaxial nanofiber Baicalin Inflammation osteoclast differentiation Vascularized bone regeneration

PIP5k1β controls bone homeostasis through modulating both osteoclast and osteoblast differentiation

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Journal of Molecular Cell Biology 2020年第1期12卷 55-70页

作者： Xiaoying Zhao Penglei Cui Guoli Hu Chuandong Wang Lei Jiang Jingyu Zhao Jiake Xu Xiaoling Zhang Department of Orthopedic Surgery Xinhua HospitalSchool of MedicineShanghai Jiao Tong UniversityShanghai 200092China The Key Laboratory of Stem Cell Biology Shanghai Institutes for Biological SciencesChinese Academy of SciencesShanghai 200025China School of Pathology and Laboratory Medicine University of Western AustraliaPerthWestern Australia6009Australia Key Laboratory of Tibetan Medicine Research Northwest Plateau Institute of BiologyChinese Academy of SciencesXining 810001China

PIP5k1βis crucial to the generation of phosphotidylinosotol(4,5)P2.PIP5k1βparticipates in numerous cellular activities,such as B cell and platelet activation,cell phagocytosis and endocytosis,cell apoptosis,and cytoskeletal organization.In the present work,we aimed to examine the function of PIP5k1βin osteoclastogenesis and osteogenesis to provide promising strategies for osteoporosis prevention and treatment.We discovered that PIP5k1β deletion in mice resulted in obvious bone loss and that PIP5k1β was highly expressed during both osteoclast and osteoblast differentiation.Deletion of the gene was found to enhance the proliferation and migration of bone marrow-derived macrophage-like cells to promote osteoclast differentiation.PIP5k1β-/-osteoclasts exhibited normal cytoskeleton architecture but stronger resorption activity.PIP5kip deficiency also promoted activation of mitogen-activated kinase and Akt signaling,enhanced TRAF6 and c-Fos expression,facilitated the expression and nuclear translocation of NFATC1,and upregulated Grb2 expression,thereby accelerating osteoclast differentiation and function.Finally,PIP5k1β enhanced osteoblast differentiation by upregulating master gene expression through triggering smad1/5/8 signaling.Therefore,PIP5k1βmodulates bone homeostasis and remodeling.

关键词： PIP5k1β osteoclast differentiation osteoblast differentiation proliferation migration NFATC1

osteoclast precursor differentiation by MCPIP via oxidative stress,endoplasmic reticulum stress,and autophagy

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分子细胞生物学报:英文版 2011年第6期3卷 360-368页

作者： Kangkai Wang Jianli Niu Hyunbae Kim Pappachan E.Kolattukudy Burnett School of Biomedical Sciences College of MedicineUniversity of Central FloridaOrlandoFL 32816USA

osteoclasts(OCs)are responsible for bone resorption in inflammatory joint diseases.Monocyte chemotactic protein-1(MCP-1)has been shown to induce differentiation of monocytes to OC precursors,but nothing is known about the underlying mechanisms.Here,we elucidate how MCPIP,induced by MCP-1,mediates this differentiation.Knockdown of MCPIP abolished MCP-1-mediated expression of OC markers,tartrate-resistant acid phosphatase,and serine protease cathepsin K.Expression of MCPIP induced p47PHOX and its membrane translocation,reactive oxygen species formation,and induction of endoplasmic reticulum(ER)stress chaperones,up-regulation of autophagy marker,Beclin-1,and lipidation of LC3,and induction of OC markers.Inhibition of oxidative stress attenuated ER stress and autophagy,and suppressed expression of OC markers.Inhibition of ER stress by a specific inhibitor or by knockdown of IRE1 blocked autophagy and induction of OC markers.ER stress inducers,tunicamycin and thapsigargin,induced expression of OC markers.Autophagy inhibition by 3′-methyladenine,LY294002,wortmannin or by knockdown of Beclin-1 or Atg 7 inhibited MCPIP-induced expression of OC markers.These results strongly suggest that MCP-1-induced differentiation of OC precursor cells is mediated via MCPIP-induced oxidative stress that causes ER stress leading to autophagy,revealing a novel mechanistic insight into the role of MCP-1 in OCs differentiation.

关键词： MCP-1 MCPIP osteoclast differentiation reactive oxygen species ER stress

MicroRNAs and their roles in osteoclast differentiation

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Frontiers of Medicine 2011年第4期5卷 414-419页

作者： Zhuying Xia Chao Chen Peng Chen Hui Xie Xianghang Luo Institute of Endocrinology and Metabolism the Second Xiangya Hospital of Central South UniversityChangsha 410011China

osteoclasts,which are derived from monocyte-macrophage precursors,are exclusive bone resorption cells.Limited evidence indicates that a class of small non-coding single-stranded RNAs known as“microRNAs”(miRNAs)is also involved in bone resorption.Although various miRNAs regulate cell proliferation and differentiation,few miRNAs have been reported to play a key role in the regulation of osteoclast differentiation.In this short review,the biology and functional mechanisms of miRNAs in osteoclastogenesis are summarized.The profiling,function,and target prediction of miRNAs are discussed as well.

关键词： miRNA osteoclast differentiation antagomirs

Inhibition Mechanism of Qingluo Tongbi Granule(清络通痹颗粒)on osteoclast differentiation Induced by Synovial Fibroblast and Monocytes Co-Culture in Adjuvant-Induced Arthritic Rats

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Chinese Journal of Integrative Medicine 2015年第4期21卷 291-298页

作者：刘天阳周玲玲周聪柳璋璞陈晨冯哲周学平 Nanjing University of Chinese Medicine Department of Rheumatology and Immunology The First Affiliated Hospital of Anhui University of Chinese Medicine

Objective： To study the mechanism underlying the inhibitory effect of Qingluo Tongbi Granule （清络通痹颗粒, QTG） on osteoclast differentiation in rheumatoid arthritis in rats. Methods： Fibroblast and monocyte co-culture were used to induce osteoclast differentiation in adjuvant-induced arthritic （AIA） rats. Serum containing QTG was prepared and added to the osteoclasts, and activation of the tumor necrosis factor receptorassociated factor 6/mitogen-activated protein kinase/nuclear factor of activated T cells, cytoplasmic1 （TRAF6/ MAPK/NFATcl） pathways was examined. Results： The induced osteoclasts were multinucleated and stained positive for tartrate-resistant acid phosphatase （TRAP） staining. Serum containing QTG at 14.4, 7.2 or 3.6 g/kg inhibited the activation of TRAF6, extracellular regulated protein kinase （ERK）1/2, c-Jun N-terminal kinase （JNK） and p38 and decreased the percentage of cells with nuclear NFATcl in a dose-dependent manner, the high and middle doses exhibited clear inhibitory activity （P〈0.01 and P〈0.05, respectively）. After the addition of MAPK inhibitors, the NFATcl expression showed no significant difference compared with the control group （P〉0.05）. Conclusions： Serum containing QTG could generally inhibit the TRAF6/MAPK pathways and possibly inhibit the NFATcl pathway. In addition, QTG may regulate other signaling pathways that are related to osteoclast differentiation and maturation.

关键词： Qingluo Tongbi Granule rheumatoid arthritis osteoclast differentiation signaling pathway,regulation of tumor necrosis factor receptor-associated factor 6/mitogen-activated protein kinase pathways,Chinese medicine

AIMP1 promotes multiple myeloma malignancy through interacting with ANP32A to mediate histone H3 acetylation

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Cancer Communications 2022年第11期42卷 1185-1206页

作者： Rongfang Wei Yan Zhu Yuanjiao Zhang Wene Zhao Xichao Yu Ling Wang Chunyan Gu Xiaosong Gu Ye Yang Nanjing Hospital of Chinese Medicine affiliated to Nanjing University of Chinese Medicine NanjingJiangsu 210001P.R.China School of Medicine&Holistic Integrative Medicine Nanjing University of Chinese MedicineNanjingJiangsu 210023P.R.China Department of Analytical and Testing Center Nanjing Medical UniversityNanjingJiangsu 211112P.R.China Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education Nantong UniversityNantongJiangsu 226019P.R.China

Background:Multiple myeloma(MM)is the second most common hematological malignancy.An overwhelming majority of patients with MM progress to serious osteolytic bone disease.Aminoacyl-tRNA synthetase-interacting multifunctional protein 1(AIMP1)participates in several steps during cancer development and osteoclast differentiation.This study aimed to explore its role in MM.Methods:The gene expression profiling cohorts of MM were applied to determine the expression of AIMP1 and its association with MM patient prognosis.Enzyme-linked immunosorbent assay,immunohistochemistry,and Western blotting were used to detect AIMP1 expression.Protein chip analysis,RNA-sequencing,and chromatin immunoprecipitation and next-generation sequencing were employed to screen the interacting proteins and key downstream targets of AIMP1.The impact of AIMP1 on cellular proliferation was determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT)assay in vitro and a xenograft model in vivo.Bone lesions were evaluated using tartrate-resistant acid phosphatase staining in vitro.A NOD/SCID-TIBIA mouse model was used to evaluate the effect of siAIMP1-loaded exosomes on bone lesion formation in vivo.Results:AIMP1 expression was increased in MM patients and strongly associated with unfavorable outcomes.Increased AIMP1 expression promoted MM cell proliferation in vitro and in vivo via activation of the mitogen-activated protein kinase(MAPK)signaling pathway.Protein chip assays and subsequent experiments revealed that AIMP1 interacted with acidic leucine-rich nuclear phosphoprotein 32 family member A(ANP32A)to regulate histone H3 acetylation.In addition,AIMP1 increased histone H3 acetylation enrichment function of GRB2-associated and regulator of MAPK protein 2(GAREM2)to increase the phosphorylation of extracellular-regulated kinase 1/2(p-ERK1/2).Furthermore,AIMP1 promoted osteoclast differentiation by activating nuclear factor of activated T cells c1(NFATc1)in vitro.In contrast,exosome-coated small interfering RNA of AIMP1 effec

关键词： multiple myeloma AIMP1 osteoclast differentiation MAPK signaling ANP32A histone H3 acetylation osteolytic lesions

Single-cell RNA sequencing reveals classical monocytes are the major precursors of rat osteoclasts

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BIOCELL 2022年第3期46卷 655-665页

作者： JIRUI WEN WENCHAO WU MIN TANG MINGYUE BAO XUELING HE XINGHONG YAO LIANG LI Institute of Biomedical Engineering West China School of Basic Medical Science and Forensic MedicineSichuan UniversityChengdu610041China Laboratory of Cardiovascular Diseases Regenerative Medicine Research CenterWest China HospitalSichuan UniversityChengdu610041China Laboratory Animal Center Sichuan UniversityChengdu610041China

To dissect which subset of bone marrow monocyte is the major precursor of osteoclast,3-month-old rat bone marrow was obtained for single-cell RNA sequencing.A total of 6091 cells were acquired for detailed analysis,with a median number of 1206 genes detected per cell and 17,959 genes detected in total.A total of 19 cell clusters were recognized,with the main lineages identified as B cells,Granulocytes,Monocytes,T cells,Erythrocytes and Macrophages.Monocytes were further divided into classical monocytes and non-classical monocytes.Compared with non-classical monocytes,classical monocytes highly expressed osteoclast differentiation related genes Mitf,Spi1,Fos and Csf1r.Additionally,biological processes of classical monocytes were related to osteoclast differentiation.qPCR revealed differentially expressed genes of classical monocytes played a role in osteoclast differentiation.In conclusion,classical monocytes were identified as the main precursors of osteoclasts in rats,and may contribute to osteoclast differentiation by regulating S100a4,S100a6,S100a10,Fn1,Vcan and Bcl2a1.The results of this study contribute to the understanding of the origin of osteoclasts and may provide potential biomarkers for early diagnosis of bone metabolic diseases,as well as molecular and cellular targets for clinical intervention in bone metabolic diseases.

关键词： Single-cell RNA sequencing Monocytes Subsets osteoclast differentiation

RANKL deletion in periodontal ligament and bone lining cells blocks orthodontic tooth movement

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International Journal of Oral Science 2018年第1期10卷 27-35页

作者： Chia-Ying Yang Hyeran Helen Jeon Ahmed Alshabab Yu Jin Lee Chun-Hsi Chung Dana T. Graves Department of Orthodontics School of Dental Medicine University of Pennsylvania Philadelphia PA USA Department of Pedodontics School of Dental Medicine University of Pennsylvania Philadelphia PA USA

The bone remodeling process in response to orthodontic forces requires the activity of osteoclasts to allow teeth to move in the direction of the force applied. Receptor activator of nuclear factor-κB ligand(RANKL) is essential for this process although its cellular source in response to orthodontic forces has not been determined. Orthodontic tooth movement is considered to be an aseptic inflammatory process that is stimulated by leukocytes including T and B lymphocytes which are presumed to stimulate bone resorption. We determined whether periodontal ligament and bone lining cells were an essential source of RANKL by tamoxifen induced deletion of RANKL in which Cre recombinase was driven by a 3.2 kb reporter element of the Col1α1 gene in experimental mice(Col1α1.CreERTM+.RANKLf/f) and compared results with littermate controls(Col1α1.CreERTM-.RANKLf/f). By examination of Col1α1.CreERTM+.ROSA26 reporter mice we showed tissue specificity of tamoxifen induced Cre recombinase predominantly in the periodontal ligament and bone lining cells. Surprisingly we found that most of the orthodontic tooth movement and formation of osteoclasts was blocked in the experimental mice, which also had a reduced periodontal ligament space. Thus, we demonstrate for the first time that RANKL produced by periodontal ligament and bone lining cells provide the major driving force for tooth movement and osteoclastogenesis in response to orthodontic forces.

关键词： DEPENDENT UP-REGULATION osteoclast differentiation ALKALINE-PHOSPHATASE MECHANICAL VIBRATION PDL FIBROBLASTS GENE-TRANSFER B-CELLS EXPRESSION TISSUE COMPRESSION

Oxidized Black Phosphorus Nanosheets as an Inorganic Antiresorptive Agent

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CCS Chemistry 2021年第4期3卷 1105-1115页

作者： Yun Xu Jianbin Mo Wei Wei Jing Zhao State Key Laboratory of Coordination Chemistry Chemistry and Biomedicine Innovation Center(ChemBIC)School of Chemistry and Chemical EngineeringNanjing UniversityNanjing 210093 State Key Laboratory of Pharmaceutical Biotechnology School of Life SciencesNanjing UniversityNanjing 210093

Black phosphorus(BP)is a newly discovered two-dimensional material that has promising applications from bioelectronics to biomedicine.However,facile oxidation of BP leads to changes in surface chemical composition and physical properties,often being referred to as the degradation process of BP.Degradation products of BP nanosheets,namely,oxidized BP nanosheets(oBPNSs),are routinely considered as by-products without many uses.Herein,we found that oBPNSs displayed excellent osteoclastogenesis inhibition effects without impairing cell viability.In contrast to the classic antiresorptive bisphosphonate drugs,oBPNSs showed a different mode of action by suppressing the maturation of osteoclasts.Bone resorption assays,osteoclast actin ring analysis,and tartrate-resistant acid phosphate activity assay results indicated that oBPNSs suppressed receptor activator of nuclear factor-κB(NF-κB)ligand(RANKL)-induced osteoclastogenesis in a dose-and oxidation-dependent manner.Transcriptomic and proteomic analyses indicated that oBPNSs inhibited the activation of the NF-κB signaling pathway and phosphorylation of mitogen-activated protein kinase(MAPK)in differentiated osteoclasts,as confirmed by Western blot analysis.Our results suggest that oBPNSs might be potential antiresorptive nanomaterials to treat osteoporosis.

关键词： oxidized black phosphorus degradation osteoclast differentiation osteoblast multiomics analysis

Identification of Potential Key Genes,miRNAs,and Pathways Involved in Pituitary Tumor Sphenoid Sinus Invasion:Bioinformatic Analysis and Machine Learning

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Identification of Potential Key Genes,miRNAs,and Pathways In...