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Biocompatible reduced graphene oxide stimulated BMSCs induce acceleration of bone remodeling and orthodontic tooth movement through promotion on osteoclastogenesis and angiogenesis

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Bioactive Materials 2022年第9期7卷 409-425页

作者： Delong Jiao Jing Wang Wenting Yu Ke Zhang Ning Zhang Lingyan Cao Xinquan Jiang Yuxing Bai Institute of Dental Research Beijing Stomatological Hospital&School of StomatologyCapital Medical UniversityBeijing100050China Department of Orthodontics Beijing Stomatological Hospital&School of StomatologyCapital Medical UniversityBeijing100050China Department of Prosthodontics Shanghai Ninth People’s HospitalShanghai Jiao Tong University School of MedicineCollege of StomatologyShanghai Jiao Tong UniversityNational Center for StomatologyNational Clinical Research Center for Oral DiseasesShanghai Key Laboratory of StomatologyShanghai Engineering Research Center of Advanced Dental Technology and MaterialsShanghai200011China

We has synthesized the biocompatible gelatin reduced graphene oxide(GOG)in previous research,and in this study we would further evaluate its effects on bone remodeling in the aspects of osteoclastogenesis and angiogenesis so as to verify its impact on accelerating orthodontic tooth movement.The mouse orthodontic tooth movement(OTM)model tests in vivo showed that the tooth movement was accelerated in the GOG local injection group with more osteoclastic bone resorption and neovascularization compared with the PBS injection group.The analysis on the degradation of GOG in bone marrow stromal stem cells(BMSCs)illustrated its good biocompatibility in vitro and the accumulation of GOG in spleen after local injection of GOG around the teeth in OTM model in vivo also didn’t influence the survival and life of animals.The co-culture of BMSCs with hematopoietic stem cells(HSCs)or human umbilical vein endothelial cells(HUVECs)in transwell chamber systems were constructed to test the effects of GOG stimulated BMSCs on osteoclastogenesis and angiogenesis in vitro.With the GOG stimulated BMSCs co-culture in upper chamber of transwell,the HSCs in lower chamber manifested the enhanced osteoclastogenesis.Meanwhile,the co-culture of GOG stimulated BMSCs with HUVECs showed a promotive effect on the angiogenic ability of HUVECs.The mechanism analysis on the biofunctions of the GOG stimulated BMSCs illustrated the important regulatory effects of PERK pathway on osteoclastogenesis and angiogenesis.All the results showed the biosecurity of GOG and the biological functions of GOG stimulated BMSCs in accelerating bone remodeling and tooth movement.

关键词： Bone remodeling Reduced graphene oxide Angiogenesis osteoclastogenesis Orthodontic tooth movement

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Nanoporous titanium implant surface promotes osteogenesis by suppressing osteoclastogenesis via integrin β1/FAKpY397/MAPK pathway

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Bioactive Materials 2022年第2期7卷 109-123页

作者： Yide He Zhe Li Xin Ding Boya Xu Jinjin Wang Yi Li Fanghao Chen Fanhui Meng Wen Song Yumei Zhang State Key Laboratory of Military Stomatology&National Clinical Research Center for Oral Diseases&Shaanxi Key Laboratory of Oral Diseases Department of ProsthodonticsSchool of StomatologyThe Fourth Military Medical UniversityXi’anChina Huaian Stomatological Hospital NanjingChina State Key Laboratory of Military Stomatology&National Clinical Research Center for Oral Diseases&Shaanxi Key Laboratory of Oral Diseases Department of PeriodontologySchool of StomatologyThe Fourth Military Medical UniversityXi’anChina State Key Laboratory of Military Stomatology Department of Dental MaterialsSchool of StomatologyThe Fourth Military Medical UniversityXi’anShaanxiChina

Macrophages and osteoclasts are both derived from monocyte/macrophage lineage,which plays as the osteoclastic part of bone metabolism.Although they are regulated by bone implant surface nanoarchitecture and involved in osseointegration,the beneath mechanism has not been simultaneously analyzed in a given surface model and their communication with osteoblasts is also blurring.Here,the effect of implant surface topography on monocyte/macrophage lineage osteoclastogenesis and the subsequent effect on osteogenesis are systematically investigated.The nanoporous surface is fabricated on titanium implant by etching and anodizing to get the nanotubes structure.The early bone formation around implant is significantly accelerated by the nanoporous surface in vivo.Meanwhile,the macrophage recruitment and osteoclast formation are increased and decreased respectively.Mechanistically,the integrin mediated FAK phosphorylation and its downstream MAPK pathway(p-p38)are significantly downregulated by the nanoporous surface,which account for the inhibition of osteoclastogenesis.In addition,the nanoporous surface can alleviate the inhibition of osteoclasts on osteogenesis by changing the secretion of clastokines,and accelerate bone regeneration by macrophage cytokine profiles.In conclusion,these data indicate that physical topography of implant surface is a critical factor modulating monocyte/macrophage lineage commitment,which provides theoretical guidance and mechanism basis for promoting osseointegration by coupling the osteogenesis and osteoclastogenesis.

关键词： Nanoporous implant Osteogenesis osteoclastogenesis FAK phosphorylation MAPK

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Mn-containing bioceramics inhibit osteoclastogenesis and promote osteoporotic bone regeneration via scavenging ROS

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Bioactive Materials 2021年第11期6卷 3839-3850页

作者： Jianmei Li Cuijun Deng Wanyuan Liang Fei Kang Yun Bai Bing Ma Chengtie Wu Shiwu Dong Department of Biomedical Materials Science School of Biomedical EngineeringThird Military Medical University(Army Medical University)Chongqing400038China State Key Laboratory of High Performance Ceramics and Superfine Microstructure Shanghai Institute of CeramicsChinese Academy of SciencesShanghai200050China State Key Laboratory of Trauma Burnsand Combined InjuryThird Military Medical University(Army Medical University)Chongqing400038China

Osteoporosis is caused by an osteoclast activation mechanism.People suffering from osteoporosis are prone to bone defects.Increasing evidence indicates that scavenging reactive oxygen species(ROS)can inhibit receptor activator of nuclear factorκB ligand(RANKL)-induced osteoclastogenesis and suppress ovariectomy-induced osteoporosis.It is critical to develop biomaterials with antioxidant properties to modulate osteoclast activity for treating osteoporotic bone defects.Previous studies have shown that manganese(Mn)can improve bone regeneration,and Mn supplementation may treat osteoporosis.However,the effect of Mn on osteoclasts and the role of Mn in osteoporotic bone defects remain unclear.In present research,a model bioceramic,Mn-containedβ-tricalcium phosphate(Mn-TCP)was prepared by introducing Mn intoβ-TCP.The introduction of Mn intoβ-TCP significantly improved the scavenging of oxygen radicals and nitrogen radicals,demonstrating that Mn-TCP bioceramics might have antioxidant properties.The in vitro and in vivo findings revealed that Mn^(2+)ions released from Mn-TCP bioceramics could distinctly inhibit the formation and function of osteoclasts,promote the differentiation of osteoblasts,and accelerate bone regeneration under osteoporotic conditions in vivo.Mechanistically,Mn-TCP bioceramics inhibited osteoclastogenesis and promoted the regeneration of osteoporotic bone defects by scavenging ROS via Nrf2 activation.These results suggest that Mn-containing bioceramics with osteoconductivity,ROS scavenging and bone resorption inhibition abilities may be an ideal biomaterial for the treatment of osteoporotic bone defect.

关键词： Mn-containing bioceramics Antioxidant biomaterials osteoclastogenesis ROS Osteoporotic bone regeneration

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Graphene oxide/gallium nanoderivative as a multifunctional modulator of osteoblastogenesis and osteoclastogenesis for the synergistic therapy of implant-related bone infection

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Bioactive Materials 2023年第7期25卷 594-614页

作者： Ying Yang Min Li Bixia Zhou Xulei Jiang Dou Zhang Hang Luo Department of Plastic Surgery Xiangya HospitalCentral South UniversityChangsha410008China State Key Laboratory of Powder Metallurgy Central South UniversityChangsha410083China Department of Oncology Changsha Central HospitalUniversity of South ChinaChangsha410006China National Clinical Research Center for Geriatric Disorders Xiangya HospitalCentral South UniversityChangsha410008China

Currently,implant-associated bacterial infections account for most hospital-acquired infections in patients suffering from bone fractures or defects.Poor osseointegration and aggravated osteolysis remain great challenges for the success of implants in infectious scenarios.Consequently,developing an effective surface modification strategy for implants is urgently needed.Here,a novel nanoplatform(GO/Ga)consisting of graphene oxide(GO)and gallium nanoparticles(GaNPs)was reported,followed by investigations of its in vitro antibacterial activity and potential bacterium inactivation mechanisms,cytocompatibility and regulatory actions on osteoblastogenesis and osteoclastogenesis.In addition,the possible molecular mechanisms underlying the regulatory effects of GO/Ga nanocomposites on osteoblast differentiation and osteoclast formation were clarified.Moreover,an in vivo infectious microenvironment was established in a rat model of implant-related femoral osteomyelitis to determine the therapeutic efficacy and biosafety of GO/Ga nanocomposites.Our results indicate that GO/Ga nanocomposites with excellent antibacterial potency have evident osteogenic potential and inhibitory effects on osteoclast differentiation by modulating the BMP/Smad,MAPK and NF-κB signaling pathways.The in vivo experiments revealed that the administration of GO/Ga nanocomposites significantly inhibited bone infections,reduced osteolysis,promoted osseointegration located in implant-bone interfaces,and resulted in satisfactory biocompatibility.In summary,this synergistic therapeutic system could accelerate the bone healing process in implant-associated infections and can significantly guide the future surface modification of implants used in bacteria-infected environments.

关键词： Nanocomposites Antimicrobial potency Implant-associated bone infections Osteogenesis osteoclastogenesis

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Calpain Inhibitor Reduces Cancer-induced Bone Pain Possibly Through Inhibition of osteoclastogenesis in Rat Cancer-induced Bone Pain Model

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Chinese Medical Journal 2015年第8期128卷 1102-1107页

作者： Jia-Ying Xu Yu Jiang Wei Liu Yu-Guang Huang Department of Anesthesiology Peking Union Medical College Hospital Chinese Academy of Medical Sciences Beijing 100730 China Department of Anesthesiology Sun Yat-sen University Cancer Center State Key Laboratory of Oncology in South China Guangzhou Guangdong 510060 China

Background： Calpain, a calcium-dependent cysteine protease, has been demonstrated to regulate osteoclastogenesis, which is considered one of the major reasons for cancer-induced bone pain （CIBP）. In the present study, calpain inhibitor was applied in a rat CIBP model to determine whether it could reduce CIBP through regulation of osteoclastogenesis activity. Methods： A rat CIBP model was established with intratibial injection of Walker 256 cells. Then, the efficacy of intraperitoneal administered calpain inhibitor III （MDL28170, 1 mg/kg） on mechanical withdrawal threshold （MWT） of bilateral hind paws was examined on postoperative days （PODs） 2, 5, 8, 11, and 14. On POD 14, the calpain inhibitor＇s effect on tumor bone tartrate-resistant acid phosphatase （TRAP） stain and radiology was also carefully investigated. Results： Pain behavioral tests in rats showed that the calpain inhibitor effectively attenuated MWTs of both the surgical side and contralateral side hind paws on POD 5, 8, and 11 （P 〈 0.05）. TRAP-positive cell count of the surgical side bone was significantly decreased in the calpain inhibitor group compared with the vehicle group （P 〈 0.05）. However, bone resorption and destruction measured by radiographs showed no difference between the two groups. Conclusions： Calpain inhibitor can effectively reduce CIBP of both the surgical side and nonsurgical side after tumor injection in a rat CIBP model. It may be due to the inhibition of receptor activator of nuclear factor-kappa B ligand-induced osteoclastogenesis. Whether a calpain inhibitor could be a novel therapeutic target to treat CIBP needs further investigation.

关键词： Calpain Cancer-induced Bone Pain Inhibitor osteoclastogenesis

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Cannabinoid receptor-2 selective antagonist negatively regulates receptor activator of nuclear factor kappa B ligand mediated osteoclastogenesis

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Chinese Medical Journal 2011年第4期124卷 586-590页

作者： GENG De-chun XU Yao-zeng YANG Hui-lin ZHU Guang-ming WANG Xian-bin ZHU Xue-song Department of Orthopaedic Surgery First Affiliated Hospital of Soochow University Suzhou Jiangsu 215006 China

Background The cannabinoid receptor-2 （CB2） is important for bone remodeling. In this study, we investigated the effects of CB2 selective antagonist （AM630） on receptor activator of nuclear factor kappa B （RANK） ligand （RANKL）induced osteoclast differentiation and the underlying signaling pathway using a monocyte-macrophage cell line-RAW264.7.Methods RAW264.7 was cultured with RANKL for 6 days and then treated with AM630 for 24 hours. Mature osteoclasts were measured by tartrate-resistant acid phosphatase （TRAP） staining using a commercial kit. Total ribonucleic acid （RNA）was isolated and real-time reverse transcriptase-polymerase chain reaction （RT-PCR） was done to examine the expression of RANK, cathepsin K （CPK） and nuclear factor kappa B （NF-κB）. The extracellular signal-regulated kinase （ERK）,phosphorylation of ERK （P-ERK） and NF-κB production were tested by Western blotting. The effect of AM630 on RAW264.7 viability was determined using the 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazoliumbromide （MTT） assay.Results AM630 did not affect the viability of RAW264.7. However, this CB2 selective antagonist markedly inhibited osteoclast formation and the inhibition rate was dose-dependent. The dose of 〉100 nmol/L could reduce TRAP positive cells to the levels that were significantly lower than the control. AM630 suppressed the expression of genes associated with osteoclast differentiation and activation, such as RANK and CPK. An analysis of a signaling pathway showed that AM630 inhibited the RANKL-induced activation of ERK, but not NF-κB.Conclusion AM630 could inhibit the osteoclastogenesis from RAW264.7 induced with RANKL.

关键词： RAW264.7 osteoclastogenesis receptor activator of nuclear factor kappa B ligand AM630,cannabinoid receptor-2

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Dolichosin A, a coumestan isolated from Glycine tabacina, inhibits IL-1β-induced inflammation in SW982 human synovial cells and suppresses RANKL-induced osteoclastogenesis: from network pharmacology to experimental pharmacology

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中国药理学与毒理学杂志 2019年第10期 910-911页

作者： TU Yan-bei WANG Kai HE Cheng-wei State Key Laboratory of Quality Research in Chinese Medicine Institute of Chinese Medical Sciences University of Macau

OBJECTIVE Dolichosins A(DoA) is a newly reported coumestan from Dolichos trilobus Linn.,however, its potential therapeutic effects on inflammatory diseases including rheumatoid arthritis(RA) are still unclear. This study aimed to investigate the anti-arthritic effects and underlying mechanisms of DoA by the integration of network pharmacology and experimental pharmacology. METHODS Putative therapeutic targets and potential pharmacological mechanisms of DoA for RA treatment were predicted by network pharmacology approach. The regulatory network of DoA acting on RA was constructed using Cytoscape 3.7.1. Anti-arthritic effects of DoA and predicted mechanisms were further validated using IL-1β-induced SW982 human synovial cell model and RANKLinduced osteoclastogenesis model. RESULTS DoA was isolated from Glycine tabacina(Labill.) Benth., a renowned Chinese medicinal herb for RA treatment, and its structure was identified by NMR and HR-ESI-MS. A total of 67 targets of DoA were predicted by inverse docking, Swiss Target Prediction and Target fishing server, and 1980 targets associated with RA pathogenesis were collected from Genecards and Dis Ge NET databases. Subsequently,a regulatory network of DoA-targets-pathways-RA was successfully constructed using network pharmacology approach. In this network, 65 candidate targets of DoA related to its therapeutic effects on RA were identified, in which NFKB1, JAK2, MAPK14, AR, MAPK8, ESR1,SRC, MAPK1 and ALB served as the hub targets, and KEGG pathway enrichment analysis revealed that these candidate targets were significantly involved in 12 central signaling pathways such as PI3 K/AKT pathway, MAPK pathway, osteoclast differentiation, Th17 cell differentiation, prolactin signaling pathway, and Th1 and Th2 cell differentiation. These results highlighted that the regulation of DoA on RA was via acting on multi-targets and multi-pathways associated with RA. In addition, the results of experimental pharmacology showed that DoA significantly inhibited IL-1β-induced inflammation in

关键词： dolichosin A rheumatoid arthritis inflammation osteoclastogenesis network pharmacology

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Bu-Shen-Ning-Xin decoction suppresses osteoclastogenesis via increasing dehydroepiandrosterone to prevent postmenopausal osteoporosis

Bu-Shen-Ning-Xin decoction suppresses osteoclastogenesis via...

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第十一届全国免疫学学术大会

作者： wang ling Laboratory for Reproductive Immunology Hospital & Institute of Obstetrics and GynecologyIBSFudan University Shanghai Medical College

Bu-Shen-Ning-Xin decoction(BSNXD), a traditional Chinese medicine, has been used to prevent and treat age-related diseases such as postmenopausal osteoporosis(PMO) for decades. This study sought to investigate the underlying mechanisms of BSNXD in terms of receptor activation of nuclear factor κB ligand(RANKL)-induced osteoclastogenesis in vitro because of the critical roles of bone resorption in the development and progression of osteoporosis. In mice, serum levels of dehydroepiandrosterone(DHEA), dehydroepiandrosterone sulfate(DHEAS), and 17-β-estradiol(E2) were evaluated with an enzyme immunoassay kit after ovariectomy. Levels of DHEA and DHEAS increased significantly following administration of BSNXD while the level of E2 did not. In addition, tartrate-resistance acid phosphatase staining showed that DHEA profoundly inhibited RANKL-induced osteoclastogenesis in vitro in a dose-dependent manner via estrogen receptor α(ERα) but not via estrogen receptor β or androgen receptors. Cytotoxicity was not detected in the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT) assay. These data suggest that BSNXD prevents PMO by increasing DHEA via the ERα pathway to suppress osteoclastogenesis.

关键词： Bu-Shen-Ning-Xin decoction DHEA osteoclastogenesis estrogen receptor α

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Bu-Shen-Ning-Xin decoction: inhibition of osteoclastogenesis by abrogation of the RANKL-induced NFATc1 and NF-κB signaling pathways via selective estrogen receptor α

Bu-Shen-Ning-Xin decoction: inhibition of osteoclastogenesis...

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第十届全国免疫学学术大会

作者： ling wang Dajin Li Hospital & Institute of Obstetrics and Gynecology IBS Fudan University Shanghai Medical College

Introduction: Bu-Shen-Ning-Xin decoction(BSNXD) is a traditional Chinese medicinal composition that has been used as a remedy for postmenopausal osteoporosis, but the mechanisms affecting bone metabolism are not fully understood.Purpose: We investigated the molecular mechanism and signaling pathway underlying the effect of BSNXD on osteoclastogenesis.Materials and Methods: A postmenopausal osteoporosis animal model generated by ovariectomywas administered BSNXD and drug-derived serum was prepared. An enzyme immunoassay was conducted to measure the 17-β-estradiol(E2) concentration in the drug-derived serum. Bone marrow-derived monocyte/macrophage precursor cells were treated with drug-derived serum, and tartrate-resistance acid phosphatase staining was conducted to observe osteoclastogenesis. A bone resorption assay was performed to analyze the effect on osteoclastic resorptive function.Real-time PCR, flow cytometry, Western blotting, transfection, and luciferase assays were conducted to explore the related mechanism.Results: E2 was not elevated in BSNXD-derived serum. BSNXD-derived serum suppressed receptor activation of nuclear factor κB ligand(RANKL)-activated osteoclastogenesis in a dose-dependent manner;this effect could be reversed by estrogen receptor α antagonist methyl-piperidino-pyrazole. The serum suppressed RANKL-induced NF-κB transcription and inhibited the accumulation of nuclear factor of activated T-cells, cytoplasmic 1 in osteoclast precursor cells;the inhibitory effect was abolished by methyl-piperidino-pyrazole but not the estrogen receptor β antagonist or androgen receptor antagonist.Conclusion: These results collectively suggest that administration of BSNXD presents inhibitoryeffects on osteoclast differentiation by abrogating the RANKL-induced nuclear factor of activated T-cells, cytoplasmic 1 and NF-κB signaling pathways downstream of estrogen receptor α,thereby contributing to the inhibitory effect on bone resorption.

关键词： herbal formula osteoclastogenesis estrogen receptor α NF-κB NFATc1

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Osthole Diminishes osteoclastogenesis through the Activation of β-Catenin-OPG Signaling in vitro

Osthole Diminishes Osteoclastogenesis through the Activation...

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第十四届全国中药和天然药物学术研讨会

作者： De-Zhi Tang Dong-Feng Zhao Zhou Yang Xiao-Feng Li Wei-Wei Da Yong-Jian Zhao Bing Shu Qi Shi Yong-Jun Wang Shanghai University of Traditional Chinese Medicine

Osthole,a coumarin-like derivative extracted from Chinese herbs,has been shown to stimulate osteoblast differentiation and bone formation.But there is no evidence to indicate the effect of Osthole on the function of osteoclast recently.To figure out the effect of Osthole on osteoclastogenesis and underlying mechanism,bone marrow mesenchymal cells(BMSCs)were harvested from 6-week-old C57BL/6 mices to perform this study.Variation doses of Osthole(0.5-5 μM) were added to indentify their effects on osteoclastogenesis and bone resorption activity.We found that,compared to the control,Osthole could inhibite the formation of osteoclast and the formation of functional osteoclast in a dose-dependent manner.We next performed qPCR analysis and found that Osthole significantly increased OPG gene expression in primary mouse BMSCs dose-dependently,especially at the dose of 100 μM.Then,BMSCs were further isolated from OPG mice and its littermates of OPG mice,induced to form osteoclast by M-CSF and RANKL,and treated with or without Osthole at the dose of 100 μM.TRAP staining data showed that Osthole reduced the number of osteoclast dramatically in OPG mice but its effect was significantly blocked in OPG’" mice,which demonstrated that Osthole inhibited osteoclast formation in an OPG-dependent manner.We also found that the deletion of the OPG gene did not affect P-catenin expression and the deletion of the p-catenin gene inhibited OPG expression in BMSCs,which demonstrated that Osthole stimulated the expression of OPG through activation of p-catenin signaling.Taken together,our findings verifyed that Osthole inhibited osteoclastogenesis by activation of P-catenin-OPG signaling and could be a potential agent to inhibit bone resorption.

关键词： Osthole β-Catenin OPG Osteoclast osteoclastogenesis Osteoporosis.

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