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| 1 | MicroRNA-145 targets vascular endothelial growth factor and inhibits invasion and metastasis of osteosarcoma cells显示文摘MicroRNAs 是在 tumorigenesis 起一个深刻作用的重要基因管理者。MicroRNA-145 (miR-145 ) ,在 microRNAs 的家庭的一个重要成员,作为肿瘤 suppressor 在肿瘤和幕的几种类型是下面表示的。角色和在 osteosarcoma carcinogenesis 的 miR-145 的可能的小径仍然是未知的。在这研究,我们发现 miR-145 在 osteosarcoma 纸巾是显著地下面表示的,并且 miR-145 的在表示上能禁止 osteosarcoma 房间的侵略和 angiopoiesis。而且,结果证明那脉管的 endothelial 生长因素(VEGF ) 表情在在 miR-145 transfection 以后的 osteosarcoma 房间是下面调整的。根据这些结果,我们执行了酶试金并且验证了那 miR-145 能在翻译水平由的下面调整 VEGF 对 VEGF 3 untranslated 区域(3UTR ) 部分有约束力。因此, miR-145 能禁止 osteosarcoma 房间的侵略和转移,这能被结束。机制之一明确地是由由到 VEGF mRNA 的 3UTR 的绑定的 miR-145 的 VEGF 表示的下面规定。这些新奇调查结果可以为 osteosarcoma 的有效基因治疗有广泛的含意。 | Qiang Wu Xiaojuan Xing Yulong Wei Zengwu Shao | 2012 | Acta Biochimica et Biophysica Sinica2012，44，5： | 18 |
| 2 | An antibody against Siglec-15 promotes bone formation and fracture healing by increasing TRAP^(+)mononuclear cells and PDGF-BB secretion显示文摘Osteoporosis(OP)is a common age-related disease characterized by a deterioration of bone mass and structure that predisposes patients to fragility fractures.Pharmaceutical therapies that promote anabolic bone formation in OP patients and OP-induced fracture are needed.We investigated whether a neutralizing antibody against Siglec-15 can simultaneously inhibit bone resorption and stimulate bone formation.We found that the multinucleation of osteoclasts was inhibited in SIGLEC-15 conditional knockout mice and mice undergoing Siglec-15 neutralizing antibody treatment.The secretion of platelet-derived growth factor-BB(PDGF-BB),the number of tartrate-resistant acid phosphatase-positive(TRAP+)mononuclear cells,and bone formation were significantly increased in the SIGLEC-15 conditional knockout mice and antibody-treated mice.The anabolic effect of the Siglec-15 neutralizing antibody on bone formation was blunted in mice with Pdgfb deleted in TRAP-1'cells.These findings showed that the anabolic effect of the Siglec-15 neutralizing antibody was mediated by elevating PDGF-BB production of TRAP4 mononuclear cells.To test the therapeutic potential of the Siglec-15 neutralizing antibody,we injected the antibody in an ovariectomy-induced osteoporotic mouse model,which mimics postmenopausal osteoporosis in women,and in two fracture healing models because fracture is the most serious health consequence of osteoporosis.The Siglec-15 neutralizing antibody effectively reduced bone resorption and stimulated bone formation in estrogen deficiency-induced osteoporosis.Of note,the Siglec-15 neutralizing antibody promoted intramembranous and endochondral ossification at the damaged area of cortical bone in fracture healing mouse models.Thus,the Siglec-15 neutralizing antibody shows significant translational potential as a novel therapy for OP and bone fracture. | Gehua Zhen Yang Dan Ruomei Wang Ce Dou Qiaoyue Guo Melissa Zarr Linda N.Liu Lieping Chen Ruoxian Deng Yusheng Li Zengwu Shao Xu Cao | 2021 | Bone Research2021，9，4： | 6 |
| 3 | Ferroptosis as a novel form of regulated cell death:Implications in the pathogenesis,oncometabolism and treatment of human cancer显示文摘The treatment of cancer mainly involves surgical excision supplemented by radiotherapy and chemotherapy.Chemotherapy drugs act by interfering with tumor growth and inducing the death of cancer cells.Anti-tumor drugs were developed to induce apoptosis,but some patient’s show apoptosis escape and chemotherapy resistance.Therefore,other forms of cell death that can overcome the resistance of tumor cells are important in the context of cancer treatment.Ferroptosis is a newly discovered iron-dependent,non-apoptotic type of cell death that is highly negatively correlated with cancer development.Ferroptosis is mainly caused by the abnormal increase in iron-dependent lipid reactive oxygen species and the imbalance of redox homeostasis.This review summarizes the progression and regulatory mechanism of ferroptosis in cancer and discusses its possible clinical applications in cancer diagnosis and treatment. | Feifei Pu Fengxia Chen Zhicai Zhang Deyao Shi Binlong Zhong Xiao Lv Andrew Blake Tucker Jiaming Fan Alexander J.Li Kevin Qin Daniel Hu Connie Chen Hao Wang Fang He Na Ni Linjuan Huang Qing Liu William Wagstaff Hue H.Luu Rex C.Haydon Le Shen Tong-Chuan He Jianxiang Liu Zengwu Shao | 2022 | Genes & Diseases2022，9，2： | 6 |
| 4 | Kindlin-2 inhibits Nlrp3 inflammasome activation in nucleus pulposus to maintain homeostasis of the intervertebral disc显示文摘Intervertebral disc(IVD) degeneration(IVDD) is the main cause of low back pain with major social and economic burdens;however, its underlying molecular mechanisms remain poorly defined. Here we show that the focal adhesion protein Kindlin-2 is highly expressed in the nucleus pulposus(NP), but not in the anulus fibrosus and the cartilaginous endplates, in the IVD tissues. Expression of Kindlin-2 is drastically decreased in NP cells in aged mice and severe IVDD patients. Inducible deletion of Kindlin-2 in NP cells in adult mice causes spontaneous and striking IVDD-like phenotypes in lumbar IVDs and largely accelerates progression of coccygeal IVDD in the presence of abnormal mechanical stress. Kindlin-2 loss activates Nlrp3 inflammasome and stimulates expression of IL-1β in NP cells, which in turn downregulates Kindlin-2. This vicious cycle promotes extracellular matrix(ECM) catabolism and NP cell apoptosis. Furthermore, abnormal mechanical stress reduces expression of Kindlin-2, which exacerbates Nlrp3 inflammasome activation, cell apoptosis, and ECM catabolism in NP cells caused by Kindlin-2 deficiency. In vivo blocking Nlrp3 inflammasome activation prevents IVDD progression induced by Kindlin-2 loss and abnormal mechanical stress. Of translational significance, adeno-associated virus-mediated overexpression of Kindlin-2 inhibits ECM catabolism and cell apoptosis in primary human NP cells in vitro and alleviates coccygeal IVDD progression caused by mechanical stress in rat. Collectively, we establish critical roles of Kindlin-2 in inhibiting Nlrp3 inflammasome activation and maintaining integrity of the IVD homeostasis and define a novel target for the prevention and treatment of IVDD. | Sheng Chen Xiaohao Wu Yumei Lai Di Chen Xiaochun Bai Sheng Liu Yongchao Wu Mingjue Chen Yuxiao Lai Huiling Cao Zengwu Shao Guozhi Xiao | 2022 | Bone Research2022，10，1： | 6 |
| 5 | Three-dimensional biofabrication of an aragoniteenriched self-hardening bone graft substitute and assessment of its osteogenicity in vitro and in vivo显示文摘A self-hardening three-dimensional(3D)-porous composite bone graft consisting of 65 wt%hydroxyapatite(HA)and 35 wt%aragonite was fabricated using a 3D-Bioplotter®.New tetracalcium phosphate and dicalcium phosphate anhydrous/aragonite/gelatine paste formulae were developed to overcome the phase separation of the liquid and solid components.The mechanical properties,porosity,height and width stability of the end products were optimised through a systematic analysis of the fabrication processing parameters including printing pressure,printing speed and distance between strands.The resulting 3D-printed bone graft was confirmed to be a mixture of HA and aragonite by X-ray diffraction,Fourier transform infrared spectroscopy and energy dispersive X-ray spectroscopy.The compression strength of HA/aragonite was between 0.56 and 2.49 MPa.Cytotoxicity was assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT)assay in vitro.The osteogenicity of HA/aragonite was evaluated in vitro by alkaline phosphatase assay using human umbilical cord matrix mesenchymal stem cells,and in vivo by juxtapositional implantation between the tibia and the anterior tibialis muscle in rats.The results showed that the scaffold was not toxic and supported osteogenic differentiation in vitro.HA/aragonite stimulated new bone formation that bridged host bone and intramuscular implants in vivo.We conclude that HA/aragonite is a biodegradable and conductive bone formation biomaterial that stimulates bone regeneration.Since this material is formed near 37°C,it will have great potential for incorporating bioactive molecules to suit personalised application;however,further study of its biodegradation and osteogenic capacity is warranted.The study was approved by the Animal Ethical Committee at Tongji Medical School,Huazhong University of Science and Technology(IACUC No.738)on October 1,2017. | Yunsong Shi Ruijun He Xiangyu Deng Zengwu Shao Davide Deganello Chunze Yan Zhidao Xia | 2020 | Biomaterials Translational2020，1，1： | 2 |
| 6 | Proper animal experimental designs for preclinical research of biomaterials for intervertebral disc regeneration显示文摘Low back pain is a vital musculoskeletal disease that impairs life quality,leads to disability and imposes heavy economic burden on the society,while it is greatly attributed to intervertebral disc degeneration(IDD).However,the existing treatments,such as medicines,chiropractic adjustments and surgery,cannot achieve ideal disc regeneration.Therefore,advanced bioactive therapies are implemented,including stem cells delivery,bioreagents administration,and implantation of biomaterials etc.Among these researches,few reported unsatisfying regenerative outcomes.However,these advanced therapies have barely achieved successful clinical translation.The main reason for the inconsistency between satisfying preclinical results and poor clinical translation may largely rely on the animal models that cannot actually simulate the human disc degeneration.The inappropriate animal model also leads to difficulties in comparing the efficacies among biomaterials in different reaches.Therefore,animal models that better simulate the clinical charateristics of human IDD should be acknowledged.In addition,in vivo regenerative outcomes should be carefully evaluated to obtain robust results.Nevertheless,many researches neglect certain critical characteristics,such as adhesive properties for biomaterials blocking annulus fibrosus defects and hyperalgesia that is closely related to the clinical manifestations,e.g,low back pain.Herein,in this review,we summarized the animal models established for IDD,and highlighted the proper models and parameters that may result in acknowledged IDD models.Then,we discussed the existing biomaterials for disc regeneration and the characteristics that should be considered for regenerating different parts of discs.Finally,well-established assays and parameters for in vivo disc regeneration are explored. | Yizhong Peng Xiangcheng Qing Hongyang Shu Shuo Tian Wenbo Yang Songfeng Chen Hui Lin Xiao Lv Lei Zhao Xi Chen Feifei Pu Donghua Huang Xu Cao Zengwu Shao | 2021 | Biomaterials Translational2021，2，2： | 2 |
| 7 | Decellularized Disc Hydrogels for hBMSCs tissue-specific differentiation and tissue regeneration显示文摘Tissue specificity,a key factor in the decellularized tissue matrix(DTM),has shown bioactive functionalities in tuning cell fate-e.g.,the differentiation of mesenchymal stem cells.Notably,cell fate is also determined by the living microenvironment,including material composition and spatial characteristics.Herein,two neighboring tissues within intervertebral discs,the nucleus pulposus(NP)and annulus fibrosus(AF),were carefully processed into DTM hydrogels(abbreviated DNP-G and DAF-G,respectively)to determine the tissue-specific effects on stem cell fate,such as specific components and different culturing methods,as well as in vivo regeneration.Distinct differences in their protein compositions were identified by proteomic analysis.Interestingly,the fate of human bone marrow mesenchymal stem cells(hBMSCs)also responds to both culturing methods and composition.Generally,hBMSCs cultured with DNP-G(3D)differentiated into NP-like cells,while hBMSCs cultured with DAF-G(2D)underwent AF-like differentiation,indicating a close correlation with the native microenvironments of NP and AF cells,respectively.Furthermore,we found that the integrin-mediated RhoA/LATS/YAP1 signaling pathway was activated in DAF-G(2D)-induced AF-specific differentiation.Additionally,the activation of YAP1 determined the tendency of NP-or AF-specific differentiation and played opposite regulatory effects.Finally,DNP-G and DAF-G specifically promoted tissue regeneration in NP degeneration and AF defect rat models,respectively.In conclusion,DNP-G and DAF-G can specifically determine the fate of stem cells through the integrin-mediated RhoA/LATS/YAP1 signaling pathway,and this tissue specificity is both compositional and spatial,supporting the utilization of tissue-specific DTM in advanced treatments of intervertebral disc degeneration. | Yizhong Peng Xiangcheng Qing Hui Lin Donghua Huang Jinye Li Shuo Tian Sheng Liu Xiao Lv Kaige Ma Rui Li Zilong Rao Ying Bai Songfeng Chen Ming Lei Daping Quan Zengwu Shao | 2021 | Bioactive Materials2021，6，10： | 1 |
| 8 | The expression of TRAIL and its receptors in osteosarcoma cells and the apoptosis effect of a combination of TRAIL, adriamycin and IFN-γ on MG-63 cells显示文摘Objective: This study investigated the effects of rh-TRAIL with or without chemotherapeutic drugs on the apoptosis of the osteosarcoma cell line, MG-63, and the influence of chemotherapeutic drugs on changes in the expression of DR5 and YinYang1(YY1) in MG-63 cells. Methods: The effects of treatment with rh-TRAIL alone and/or chemotherapeutic drugs on MG-63 cell growth inhibition and apoptosis were measured using the MTT assay, FACS analysis of Annexin V labeled cells, and the mRNA changes of DR5 and YY1 were detected by RT-PCR. Results: Rh-TRAIL protein inhibited the growth of MG-63 cells, and this inhibition was increased by adriamycin and IFN-γ. Adriamycin and IFN-γ significantly facilitated the induction of the expression of DR5 and reduced the expression of YY1. Conclusion: The apoptosis-inducing effect of rh-TRAIL in MG-63 cells was enhanced by chemotherapeutic drugs. | Chao Deng Zengwu Shao Xiaoqian Xiong Zhichuan Liu Zhicai Zhang | 2009 | Journal of Nanjing Medical University2009，23，4： | 1 |
| 9 | Endogenous repair theory enriches construction strategies for orthopaedic biomaterials:a narrative review显示文摘The development of tissue engineering has led to new strategies for mitigating clinical problems;however,the design of the tissue engineering materials remains a challenge.The limited sources and inadequate function,potential risk of microbial or pathogen contamination,and high cost of cell expansion impair the efficacy and limit the application of exogenous cells in tissue engineering.However,endogenous cells in native tissues have been reported to be capable of spontaneous repair of the damaged tissue.These cells exhibit remarkable plasticity,and thus can differentiate or be reprogrammed to alter their phenotype and function after stimulation.After a comprehensive review,we found that the plasticity of these cells plays a major role in establishing the cell source in the mechanism involved in tissue regeneration.Tissue engineering materials that focus on assisting and promoting the natural self-repair function of endogenous cells may break through the limitations of exogenous seed cells and further expand the applications of tissue engineering materials in tissue repair.This review discusses the effects of endogenous cells,especially stem cells,on injured tissue repairing,and highlights the potential utilisation of endogenous repair in orthopaedic biomaterial constructions for bone,cartilage,and intervertebral disc regeneration. | Yizhong Peng Jinye Li Hui Lin Shuo Tian Sheng Liu Feifei Pu Lei Zhao Kaige Ma Xiangcheng Qing Zengwu Shao | 2021 | Biomaterials Translational2021，2，4： | 1 |
| 10 | Adenovirus-mediated tissue inhibitor of metalloproteinase-3 gene transfection inhibits rabbit intervertebral disc degeneration in vivo显示文摘The aim of this study was to investigate the inhibitory effects of recombinant adenovirus vector carrying tissue inhibitor of metalloproteinase-3(RAd-TIMP-3)against degeneration of rabbit intervertebral disc.Thirty Japanese white rabbits of 4 months old were randomly divided into 5 groups.Mild or moderate rabbit lumbar disc degeneration model was constructed with the controllable axial loading device by imposing 98 N pressure at the discs for 2 weeks.Various doses of virus were injected into the degenerated discs as follows:20μL of normal saline in group 1;20μL of RAd66(an empty adenovirus vector,1.0�1010 OPU/mL)in group 2;and 20,10,and 5μL of RAdTIMP-3(1.0�1010 OPU/mL)in groups 3,4,and 5,respectively.Two weeks after the injection,the discs were collected for investigations,including assessment of degeneration degrees according to the Thompson’s grading system,reverse-transcription polymerase chain reaction(RT-PCR)assay for TIMP-3 gene,Safranin O-Fast green staining,and immunohisto-chemical staining for TIMP-3 and type II collagen.According to Thompson’s criteria,the degeneration of groups 3,4,and 5,especially group 3,was alleviated as compared with groups 1 and 2.RT-PCR revealed that the expression of TIMP-3 in groups 3,4,and 5,especially in group 3,was significantly enhanced as compared with group 1(P<0.01).Both Safranin O-Fast green staining and type II collagen staining demonstrated better reserved integrity of disc matrix in groups 3,4,and 5 than in groups 1 and 2.TIMP-3 staining exhibited an obvious increase of positive-staining rate in groups 3,4,and 5 as compared with group 1.The positive-staining rate in group 3(79.42%�1.35%)was about 3 times that of group 1(25.47%�5.46%,P<0.01).RAdTIMP-3 can effectively protect the matrix of rabbit intervertebral disc against overloading-induced degeneration in a dose-dependent manner,resulting in the alleviation of disc degeneration. | Xudong YU Zengwu SHAO Liming XIONG Weiwei XU Hezhong WANG Huifa XU | 2009 | Frontiers of Medicine2009，3，4： | 1 |
| 11 | Characterizing the tumor microenvironment at the single-cell level reveals a novel immune evasion mechanism in osteosarcoma显示文摘The immune microenvironment extensively participates in tumorigenesis as well as progression in osteosarcoma(OS).However,the landscape and dynamics of immune cells in OS are poorly characterized.By analyzing single-cell RNA sequencing(sc RNA-seq)data,which characterize the transcription state at single-cell resolution,we produced an atlas of the immune microenvironment in OS.The results suggested that a cluster of regulatory dendritic cells(DCs)might shape the immunosuppressive microenvironment in OS by recruiting regulatory T cells.We also found that major histocompatibility complex class I(MHC-I)molecules were downregulated in cancer cells.The findings indicated a reduction in tumor immunogenicity in OS,which can be a potential mechanism of tumor immune escape.Of note,CD24 was identified as a novel“don’t eat me”signal that contributed to the immune evasion of OS cells.Altogether,our findings provide insights into the immune landscape of OS,suggesting that myeloid-targeted immunotherapy could be a promising approach to treat OS. | Weijian Liu Hongzhi Hu Zengwu Shao Xiao Lv Zhicai Zhang Xiangtian Deng Qingcheng Song Yong Han Tao Guo Liming Xiong Baichuan Wang Yingze Zhang | 2023 | Bone Research2023，11，1： | 1 |
| 12 | Traumatic brain injury stimulates sympathetic tone-mediated bone marrow myelopoiesis to favor fracture healing显示文摘Traumatic brain injury(TBI)accelerates fracture healing,but the underlying mechanism remains largely unknown.Accumulating evidence indicates that the central nervous system(CNS)plays a pivotal role in regulating immune system and skeletal homeostasis.However,the impact of CNS injury on hematopoiesis commitment was overlooked.Here,we found that the dramatically elevated sympathetic tone accompanied with TBI-accelerated fracture healing;chemical sympathectomy blocks TBIinduced fracture healing.TBI-induced hypersensitivity of adrenergic signaling promotes the proliferation of bone marrow hematopoietic stem cells(HSCs)and swiftly skews HSCs toward anti-inflammation myeloid cells within 14 days,which favor fracture healing.Knockout ofβ3-orβ2-adrenergic receptor(AR)eliminate TBI-mediated anti-inflammation macrophage expansion and TBIaccelerated fracture healing.RNA sequencing of bone marrow cells revealed that Adrb2 and Adrb3 maintain proliferation and commitment of immune cells.Importantly,flow cytometry confirmed that deletion ofβ2-AR inhibits M2 polarization of macrophages at 7th day and 14th day;and TBI-induced HSCs proliferation was impaired inβ3-AR knockout mice.Moreover,β3-andβ2-AR agonists synergistically promote infiltration of M2 macrophages in callus and accelerate bone healing process.Thus,we conclude that TBI accelerates bone formation during early stage of fracture healing process by shaping the anti-inflammation environment in the bone marrow.These results implicate that the adrenergic signals could serve as potential targets for fracture management. | Weijian Liu Wei Chen Mao Xie Chao Chen Zengwu Shao Yiran Zhang Haiyue Zhao Qingcheng Song Hongzhi Hu Xin Xing Xianyi Cai Xiangtian Deng Xinyan Li Peng Wang Guohui Liu Liming Xiong Xiao Lv Yingze Zhang | 2023 | Signal Transduction and Targeted Therapy2023，8，8： | 1 |
| 13 | Kindlin-2 regulates skeletal homeostasis by modulating PTH1R in mice显示文摘In vertebrates,the type 1 parathyroid hormone receptor(PTH1R)is a critical regulator of skeletal development and homeostasis;however,how it is modulated is incompletely understood.Here we report that deleting Kindlin-2 in osteoblastic cells using the mouse 10-kb Dmp1-Cre largely neutralizes the intermittent PTH-stimulated increasing of bone volume fraction and bone mineral density by impairing both osteoblast and osteoclast formation in murine adult bone.Single-cell profiling reveals that Kindlin-2 loss increases the proportion of osteoblasts,but not mesenchymal stem cells,chondrocytes and fibroblasts,in non-hematopoietic bone marrow cells,with concomitant depletion of osteoblasts on the bone surfaces,especially those stimulated by PTH.Furthermore,haploinsufficiency of Kindlin-2 and Pth1r genes,but not that of either gene,in mice significantly decreases basal and,to a larger extent,PTH-stimulated bone mass,supporting the notion that both factors function in the same genetic pathway.Mechanistically,Kindlin-2 interacts with the C-terminal cytoplasmic domain of PTH1R via aa 474–475 and Gsα.Kindlin-2 loss suppresses PTH induction of cAMP production and CREB phosphorylation in cultured osteoblasts and in bone.Interestingly,PTH promotes Kindlin-2 expression in vitro and in vivo,thus creating a positive feedback regulatory loop.Finally,estrogen deficiency induced by ovariectomy drastically decreases expression of Kindlin-2 protein in osteocytes embedded in the bone matrix and Kindlin-2 loss essentially abolishes the PTH anabolic activity in bone in ovariectomized mice.Thus,we demonstrate that Kindlin-2 functions as an intrinsic component of the PTH1R signaling pathway in osteoblastic cells to regulate bone mass accrual and homeostasis. | Xuekun Fu Bo Zhou Qinnan Yan Chu Tao Lei Qin Xiaohao Wu Sixiong Lin Sheng Chen Yumei Lai Xuenong Zou Zengwu Shao Meiqing Wang Di Chen Wenfei Jin Youqiang Song Huiling Cao Ge Zhang Guozhi Xiao | 2020 | Signal Transduction and Targeted Therapy2020，5，1： | 0 |
| 14 | Three-dimensional-printed titanium prostheses with bone trabeculae enable mechanical-biological reconstruction after resection of bone tumours显示文摘Reconstruction after resection has always been an urgent problem in the treatment of bone tumours.There are many methods that can be used to reconstruct bone defects;however,there are also many complications,and it is difficult to develop a safe and effective reconstruction plan for the treatment of bone tumours.With the rapid development of digital orthopaedics,three-dimensional printing technology can solve this problem.The three-dimensional printing of personalised prostheses has many advantages.It can be used to print complex structures that are difficult to fabricate using traditional processes and overcome the problems of stress shielding and low biological activity of conventional prostheses.In this study,12 patients with bone tumours were selected as research subjects,and based on individualised reverse-engineering design technology,a three-dimensional model of each prosthesis was designed and installed using medical image data.Ti6Al4V was used as the raw material to prepare the prostheses,which were used to repair bone defects after surgical resection.The operation time was 266.43±21.08 minutes(range 180-390 minutes),and intraoperative blood loss was 857.26±84.28 mL(range 800-2500 mL).One patient had delayed wound healing after surgery,but all patients survived without local tumour recurrence,and no tumour metastasis was found.No aseptic loosening or structural fracture of the prosthesis,and no non-mechanical prosthesis failure caused by infection,tumour recurrence,or progression was observed.The Musculo-Skeletal Tumour Society(MSTS)score of limb function was 22.53±2.09(range 16-26),and ten of the 12 patients scored≥20 and were able to function normally.The results showed that three-dimensional printed prostheses with an individualised design can achieve satisfactory short-term clinical efficacy in the reconstruction of large bone defects after bone tumour resection. | Feifei Pu Wei Wu Doudou Jing Yihan Yu Yizhong Peng Jianxiang Liu Qiang Wu Baichuan Wang Zhicai Zhang Zengwu Shao | 2022 | Biomaterials Translational2022，3，2： | 0 |
| 15 | Engineered microorganisms-based delivery systems for targeted cancer therapy:a narrative review显示文摘Microorganisms with innate and artificial advantages have been regarded as intelligent drug delivery systems for cancer therapy with the help of engineering technology.Although numerous studies have confirmed the promising prospects of microorganisms in cancer,several problems such as immunogenicity and toxicity should be addressed before further clinical applications.This review aims to investigate the developments of engineered microorganisms-based delivery systems for targeted cancer therapy.The main types and characteristics of microorganisms such as bacteria,viruses,fungi,microalgae,and their components are introduced in detail.Moreover,the engineering strategies and biomaterials design of microorganisms are further discussed.Most importantly,we discussed the innovative attempts and therapeutic effects of engineered microorganisms in cancer.Taken together,engineered microorganisms-based delivery systems hold tremendous prospects for biomedical applications in targeted cancer therapy. | Xin Huang Haoyu Guo Lutong Wang Zengwu Shao | 2022 | Biomaterials Translational2022，3，3： | 0 |
| 16 | Development of porphyrin and titanium dioxide sonosensitizers for sonodynamic cancer therapy显示文摘Sonodynamic therapy for malignant tumours has gained much attention for its deep penetration effect and efficient tumour killing ability.The design,modification,and utilization of sonosensitizers are important aspects of sonodynamic therapy.As an essential factor in this process,highly effective sonosensitizers should be developed to facilitate the clinical applications of sonodynamic therapy.This review takes porphyrin-and titanium dioxide(TiO_(2))-based systems as representative organic and inorganic sonosensitizers respectively,and summarizes their characteristics and biological effects as sonodynamic therapy.Upon discovery of novel sonosensitizers,sonodynamic therapy becomes an efficient means of adjuvant therapy for the treatment of malignant tumours. | Xiangyu Deng Zengwu Shao Yanli Zhao | 2021 | Biomaterials Translational2021，2，1： | 0 |
| 17 | Kindlin-2 regulates skeletal homeostasis by modulating PTH1R in mice显示文摘In vertebrates,the type 1 parathyroid hormone receptor(PTH1R)is a critical regulator of skeletal development and homeostasis;however,how it is modulated is incompletely understood.Here we report that deleting Kindlin-2 in osteoblastic cells using the mouse 10-kb Dmp1-Cre largely neutralizes the intermittent PTH-stimulated increasing of bone volume fraction and bone mineral density by impairing both osteoblast and osteoclast formation in murine adult bone.Single-cell profiling reveals that Kindlin-2 loss increases the proportion of osteoblasts,but not mesenchymal stem cells,chondrocytes and fibroblasts,in non-hematopoietic bone marrow cells,with concomitant depletion of osteoblasts on the bone surfaces,especially those stimulated by PTH.Furthermore,haploinsufficiency of Kindlin-2 and Pth1r genes,but not that of either gene,in mice significantly decreases basal and,to a larger extent,PTH-stimulated bone mass,supporting the notion that both factors function in the same genetic pathway.Mechanistically,Kindlin-2 interacts with the C-terminal cytoplasmic domain of PTH1R via aa 474–475 and Gsα.Kindlin-2 loss suppresses PTH induction of cAMP production and CREB phosphorylation in cultured osteoblasts and in bone.Interestingly,PTH promotes Kindlin-2 expression in vitro and in vivo,thus creating a positive feedback regulatory loop.Finally,estrogen deficiency induced by ovariectomy drastically decreases expression of Kindlin-2 protein in osteocytes embedded in the bone matrix and Kindlin-2 loss essentially abolishes the PTH anabolic activity in bone in ovariectomized mice.Thus,we demonstrate that Kindlin-2 functions as an intrinsic component of the PTH1R signaling pathway in osteoblastic cells to regulate bone mass accrual and homeostasis. | Xuekun Fu Bo Zhou Qinnan Yan Chu Tao Lei Qin Xiaohao Wu Sixiong Lin Sheng Chen Yumei Lai Xuenong Zou Zengwu Shao Meiqing Wang Di Chen Wenfei Jin Youqiang Song Huiling Cao Ge Zhang Guozhi Xiao | 2021 | Signal Transduction and Targeted Therapy2021，6，1： | 0 |
| 18 | Corrigendum to‘Decellularized disc hydrogels for hBMSC tissue-specific differentiation and tissue regeneration’[Bioactive Materials 6(2021)3541-3556]显示文摘The authors regret missing out the below change in the acknowledgment section of the article.The original sentence reads as'This work was supported by the Major Research Plan of National Natural Science Foundation of China[No.91649204],the National Key Research and Development Program of China[2016YFC1100100],…'and the same has been corrected to'This work was supported by the National Key Research and Development Program of China[2016YFC1100100],the Major Research Plan of National Natural Science Foundation of China[No.91649204],…'and the same has been corrected to'This work was supported by the National Key Research and Development Program of China[2016YFC1100100],the Major Research Plan of National Natural Science Foundation of China[No.91649204],…'. | Yizhong Peng Xiangcheng Qing Hui Lin Donghua Huang Jinye Li Shuo Tian Sheng Liu Xiao Lv Kaige Ma Rui Li Zilong Rao Ying Bai Songfeng Chen Ming Lei Daping Quan Zengwu Shao | 2022 | Bioactive Materials2022，7，2： | 0 |
| 19 | Roles of focal adhesion proteins in skeleton and diseases显示文摘The skeletal system,which contains bones,joints,tendons,ligaments and other elements,plays a wide variety of roles in body shaping,support and movement,protection of internal organs,production of blood cells and regulation of calcium and phosphate metabolism.The prevalence of skeletal diseases and disorders,such as osteoporosis and bone fracture,osteoarthritis,rheumatoid arthritis,and intervertebral disc degeneration,increases with age,causing pain and loss of mobility and creating a huge social and economic burden globally.Focal adhesions(FAs)are macromolecular assemblies that are composed of the extracellular matrix(ECM),integrins,intracellular cytoskeleton and other proteins,including kindlin,talin,vinculin,paxillin,pinch,Src,focal adhesion kinase(FAK)and integrin-linked protein kinase(ILK)and other proteins.FA acts as a mechanical linkage connecting the ECM and cytoskeleton and plays a key role in mediating cell–environment communications and modulates important processes,such as cell attachment,spreading,migration,differentiation and mechanotransduction,in different cells in skeletal system by impacting distinct outside-in and inside-out signaling pathways.This review aims to integrate the up-to-date knowledge of the roles of FA proteins in the health and disease of skeletal system and focuses on the specific molecular mechanisms and underlying therapeutic targets for skeletal diseases. | Sheng Chen Tailin He Yiming Zhong Mingjue Chen Qing Yao Di Chen Zengwu Shao Guozhi Xiao | 2023 | Acta Pharmaceutica Sinica B2023，13，3： | 0 |
| 20 | Corrigendum to'Cellular senescence-driven transcriptional reprogramming of the MAFB/NOTCH3 axis activates the PI3K/AKT pathway and promotes osteosarcoma progression'[Genes&Diseases 11(2024)952-963]显示文摘The authors regret that some data errors were made in'Cellular senescence-driven transcriptional reprogramming of the MAFB/NOTCH3 axis activates the PI3K/AKT pathway and promotes osteosarcoma progression'at Figure 5F for the colony formation of MNNG/HOS cells with si-NOTCH3 and 5G for the tranwell assay of U2OS cells with si-NOCTH3.Correction and supplementation to Figure 5.The author used confusing experimental data and did not notice these errors when submitting the original manuscript.Here,the authors made the latest corrections to the data of the batch of U2OS cells and MNNG/HOS cells transfected with si-NoTCH3.The authors confirm that this correction will not alter the conclusions in the original manuscript. | Zhenhao Zhang Doudou Jing Baijun Xuan Zhicai Zhang Wei Wu Zengwu Shao | 2024 | Genes & Diseases2024，11，3： | 0 |
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