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Lanthanum promoting bone formation by regulating osteogenesis,osteoclastogenesis and angiogenesis

Journal of Rare Earths 2024年第3期42卷 621-628,I0007页

作者： Dandan Zou Runlian Lin Yu Han Juan Jia Guoqiang Zhou Haisong Zhang Kun Ge Hebei Key laboratory of Chronic Kidney Diseases and bone metabolism Affiliated Hospital of Hebei UniversityBaoding071000China Key laboratory of Medicinal Chemistry and Molecular Diagnosis of the Ministry of Education Key Laboratory of Chemical Biology of Hebei ProvinceCollege of Chemistry and Environmental ScienceHebei UniversityBaoding071002China

With lanthanum(La) in agriculture, medicine, and the chemical industry, La shows accumulation in the body, especially in the bone, because of its similar structure to calcium. Moreover, La has a direct role in bone formation regulating osteoblasts and osteoclasts. Nevertheless, bone formation is complex under the regulation of osteogenesis, osteoclastogenesis, and angiogenesis in the bone microenvironment. It is difficult to comprehensively understand the regulation of bone homeostasis from a single kind of ***, some bone microenvironment-related cells and mouse calvaria culture models were used to study the regulatory effect of La-based compound-lanthanum nitrate(La(NO_(3))_(3)) on bone ***(NO_(3))_(3) has good biological safety, and the osteogenic differentiation is significantly increased under La(NO_(3))_(3) treatment for bone marrow mesenchymal stem cells(BMMSC). In contrast, the differentiation,maturation, and bone erosion ability of osteoclasts are significantly decreased. Meanwhile, the angiogenesis ability of human umbilical vein endothelial cells(HUVEC) is significantly promoted when treated with La(NO_(3))_(3). Furthermore, bone metabolism and angiogenesis are improved under La(NO_(3))_(3) treatment in the calvaria ex vivo culture model and BMMSC-HUVEC co-culture system. These results suggest that La has the beneficial effect of promoting bone metabolism and improving bone formation in the bone microenvironment.

关键词： Lanthanum bone microenvironment Osteogenic differentiation Angiogenesis Rare earths

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bone remodeling:an operational process ensuring survival and bone mechanical competence

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bone Research 2022年第3期10卷 421-439页

作者： Simona Bolamperti Isabella Villa Alessandro Rubinacci Osteoporosis and bone and Mineral metabolism Unit IRCCS San Raffaele HospitalVia Olgettina 6020132 MilanoItaly

bone remodeling replaces old and damaged bone with new bone through a sequence of cellular events occurring on the same surface without any change in bone shape. It was initially thought that the basic multicellular unit(BMU) responsible for bone remodeling consists of osteoclasts and osteoblasts functioning through a hierarchical sequence of events organized into distinct stages. However, recent discoveries have indicated that all bone cells participate in BMU formation by interacting both simultaneously and at different differentiation stages with their progenitors, other cells, and bone matrix constituents. Therefore,bone remodeling is currently considered a physiological outcome of continuous cellular operational processes optimized to confer a survival advantage. bone remodeling defines the primary activities that BMUs need to perform to renew successfully bone structural units. Hence, this review summarizes the current understanding of bone remodeling and future research directions with the aim of providing a clinically relevant biological background with which to identify targets for therapeutic strategies in osteoporosis.

关键词： remodeling replace initially

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Endogenous Glucocorticoids and bone

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bone Research 2013年第2期1卷 107-119页

作者： Hong Zhou Mark S. Cooper Markus J. Seibel bone Research Program ANZAC Research Institute Concord Clinical School The University of Sydney Department of Endocrinology & metabolism Concord Hospital

While the adverse effects of glucocorticoids on bone are well described, positive effects of glucocorticoids on the differentiation of osteoblasts are also observed. These paradoxical effects of glucocorticoids are dose dependent. At both physiologicaland supraphysiological levels of glucocorticoids, osteoblasts and osteocytes are the major glucocorticoid target cells. However, the response of the osteoblasts to each of these is quite distinct. At physiology levels, glucocorticoids direct mesenchymal progenitor cells to differentiate towards osteoblasts and thus increase bone formation in a positive way. In contrast with ageing, the excess production of glucocorticoids, at both systemic and intracellular levels, appear to impact on osteoblast and osteocytes in a negative way in a similar fashion to that seen with therapeutic glucocorticoids. This review will focus on therole of glucocorticoids in normal bone physiology, with particular emphasis on the mechanism by which endogenous glucocorticoids impact on bone and its constituent cells.

关键词： glucocorticoids mechanisms of action bone osteoblasts skeletal development Wnt signaling

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The role of 5′-adenosine monophosphate-activated protein kinase(AMPK)in skeletal muscle atrophy

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BIOCELL 2023年第2期47卷 269-281页

作者： KAI DANG HAFIZ MUHAMMAD UMER FAROOQ YUAN GAO XIAONI DENG AIRONG QIAN laboratory for bone metabolism Xi’an Key Laboratory of Special Medicine and Health EngineeringKey Laboratory for Space Biosciences and BiotechnologyResearch Center for Special Medicine and Health Systems EngineeringNPU-UAB Joint Laboratory for Bone MetabolismSchool of Life SciencesNorthwestern Polytechnical UniversityXi’an710072China

As a key coordinator of metabolism,AMP-activated protein kinase(AMPK)is vitally involved in skeletal muscle *** exerts its cellular effects through its function as a serine/threonine protein kinase by regulating many downstream targets and plays important roles in the development and growth of skeletal *** is activated by phosphorylation and exerts its function as a kinase in many processes,including synthesis and degradation of proteins,mitochondrial biogenesis,glucose uptake,and fatty acid and cholesterol *** muscle atrophy is a result of various diseases or disorders and is characterized by a decrease in muscle *** pathogenesis and therapeutic strategies of skeletal muscle atrophy are still under *** this review,we discuss the role of AMPK in skeletal muscle metabolism and *** also discuss targeting AMPK for skeletal muscle treatment,including exercise,AMPK activators including 5-amino-4-imidazolecarboxamide ribonucleoside and metformin,and low-level *** studies show the important roles of AMPK in regulating muscle metabolism and function;thus,the treatment of skeletal muscle atrophy needs to take into account the roles of AMPK.

关键词： AMPK,Autophagy Protein degradation,Protein synthesis,Skeletal muscle atrophy,Ubiquitin

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De novo serine synthesis regulates chondrocyte proliferation during bone development and repair

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bone Research 2022年第2期10卷 274-285页

作者： Steve Stegen Shauni Loopmans Ingrid Stockmans Karen Moermans Peter Carmeliet Geert Carmeliet laboratory of Clinical and Experimental Endocrinology Department of Chronic Diseases and MetabolismKU Leuven3000 LeuvenBelgium laboratory of Angiogenesis and Vascular metabolism VIB Center for Cancer Biology3000 LeuvenBelgium laboratory of Angiogenesis and Vascular metabolism Department of Oncology and Leuven Cancer InstituteKU Leuven3000 LeuvenBelgium State Key laboratory of Ophthalmology Zhongshan Ophthalmic CenterSun Yat-Sen UniversityGuangzhou 510080China

The majority of the mammalian skeleton is formed through endochondral ossification starting from a cartilaginous *** cells, or chondrocytes, survive, proliferate and synthesize extracellular matrix in an avascular environment, but the metabolic requirements for these anabolic processes are not fully understood. Here, using metabolomics analysis and genetic in vivo models, we show that maintaining intracellular serine homeostasis is essential for chondrocyte function. De novo serine synthesis through phosphoglycerate dehydrogenase(PHGDH)-mediated glucose metabolism generates nucleotides that are necessary for chondrocyte proliferation and long bone growth. On the other hand, dietary serine is less crucial during endochondral bone formation, as serine-starved chondrocytes compensate by inducing PHGDH-mediated serine ***, this metabolic flexibility requires ATF4, a transcriptional regulator of amino acid metabolism and stress *** demonstrate that both serine deprivation and PHGDH inactivation enhance ATF4 signaling to stimulate de novo serine synthesis and serine uptake, respectively, and thereby prevent intracellular serine depletion and chondrocyte dysfunction. A similar metabolic adaptability between serine uptake and de novo synthesis is observed in the cartilage callus during fracture ***, the results of this study reveal a critical role for PHGDH-dependent serine synthesis in maintaining intracellular serine levels under physiological and serine-limited conditions, as adequate serine levels are necessary to support chondrocyte proliferation during endochondral ossification.

关键词： synthesis starting thereby

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Wnt/β-catenin signaling components and mechanisms in bone formation,homeostasis,and disease

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bone Research 2024年第3期12卷 469-501页

作者： Lifang Hu Wei Chen Airong Qian Yi-Ping Li laboratory for bone metabolism Xi’an Key Laboratory of Special Medicine and Health EngineeringKey Laboratory for Space Biosciences and BiotechnologyResearch Center for Special Medicine and Health Systems EngineeringSchool of Life SciencesNorthwestern Polytechnical UniversityXi’anShaanxi710072China Division in Cellular and Molecular Medicine Department of Pathology and Laboratory MedicineTulane University School of MedicineTulane UniversityNew OrleansLA70112USA

Wnts are secreted,lipid-modified proteins that bind to different receptors on the cell surface to activate canonical or non-canonical Wnt signaling pathways,which control various biological processes throughout embryo... 详细信息

关键词： homeostasis canonical mechanisms

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Advances in murine models of breast cancer bone disease

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Journal of Cancer Metastasis and Treatment 2021年第1期7卷 158-177页

作者： Penelope D.Ottewell Michelle A.Lawson Department of Oncology and metabolism Mellanby Centre for Bone ResearchUniversity of SheffieldSheffield S102RXUK

bone is the most prevalent metastatic site for breast cancer affecting~70%of patients with late-stage *** for this condition currently focus on controlling disease progression and limiting tumour-induced damage to bone,thereby playing a valuable role in increasing quality of ***,limited understanding of the interplay between tumour cells and their environment during bone metastasis has impeded the development of curative *** unravel the complex genetic and phenotypic alterations that occur during this process,it would be helpful to have a model in which tumours develop spontaneously at the primary site,spread to bone,undergo a dormancy phase and then,after a fixed timeframe,become re-activated to form osteolytic/mixed lesions in the *** humans,spontaneous metastasis of primary mammary tumours to bone is rare in mice and no syngeneic models of oestrogen receptor positive disease have been *** there is no single model that authentically reproduces all of the genetic and phenotypic changes representative of human bone metastasis,this review discusses the traditional and novel mouse models that are used to study bone metastasis from breast ***,this review focuses on advances that have been made towards making these models more closely related to human disease in an attempt to help researchers select the correct model(s)for their experimental needs with the aim of improving translational efficacy between the laboratory and the clinic.

关键词： Breast cancer bone metastasis mouse models

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Mechanical Sensitive Molecule MACF1 Promotes Osteoblast Differentiation

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医用生物力学 2019年第A1期34卷 71-72页

作者： Lifang Hu Chong Yin Zixiang Wu Zizhang Huang Peihong Su Yan Zhang Zhihao Chen Airong Qian Lab for bone metabolism Key Lab for Space Biosciences and BiotechnologyResearch Center for Special Medicine and Health Systems EngineeringNPU-UAB Joint Laboratory for Bone MetabolismSchool of Life SciencesNorthwestern Polytechnical University

The decreased osteoblast differentiation associated with reduced bone formation is one main cause of microgravityinduced bone *** previous studies have demonstrated that microtubule actin crosslinking factor 1(MACF1)is downregulated in association with the decreased osteoblast differentiation and bone formation under simulated microgravity *** findings suggest that MACF1 is sensitive to mechanical condition and may be critical for osteoblast differentiation and bone *** verify this hypothesis,current study investigates the role and mechanism of MACF1 in regulatingosteoblast differentiation by adopting MACF1 knockdown(MACF1-KD)*** results showed that MACF1 knockdown suppressed mineralized nodules formation,alkaline phosphatase(ALP)activity,osteogenic gene expression andβ-catenin signaling ***,we used RNA sequencing(RNA-seq)and chromatin immunoprecipitation sequencing(ChIP-seq)to investigate further ***,we found that MACF1 sequesterd repressors of osteoblast differentiation in *** conclusion,MACF1 is sensitive to mechanical condition and plays key role in activatingβ-catenin signaling transduction and sequestering repressors of osteoblast differentiation,which further promotes osteoblast differentiation.

关键词： MACF1 osteoblast cell differentiation β-catenin signaling

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The role of E3 ubiquitin ligases in bone homeostasis and related diseases

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Acta Pharmaceutica Sinica B 2023年第10期13卷 3963-3987页

作者： Yuechao Dong Yangshan Chen Guixing Ma Huiling Cao Department of Biochemistry School of MedicineSouthern University of Science and TechnologyGuangdong Provincial Key Laboratory of Cell Microenvironment and Disease ResearchKey University Laboratory of Metabolism and Health of GuangdongShenzhen 518055China

The ubiquitin-proteasome system(UPS)dedicates to degrade intracellular proteins to modulate demic homeostasis and functions of *** enzymatic cascades mark and modifies target proteins diversly through covalently binding ubiquitin *** the UPS,E3 ubiquitin ligases are the crucial constituents by the advantage of recognizing and presenting proteins to proteasomes for *** the major regulators of protein homeostasis,E3 ligases are indispensable to proper cell manners in diverse systems,and they are well described in physiological bone growth and bone ***,classic bone-related diseases such as metabolic bone diseases,arthritis,bone neoplasms and bone metastasis of the tumor,etc.,were also depicted in a UPS-dependent ***,skeletal system is versatilely regulated by UPS and it is worthy to summarize the underlying ***,based on the current status of treatment,normal or pathological osteogenesis and tumorigenesis elaborated in this review highlight the clinical significance of UPS *** a strategy possibly remedies the limitations of UPS treatment,emerging PROTAC was described comprehensively to illustrate its potential in clinical ***,the purpose of this review aims to provide more evidence for exploiting novel therapeutic strategies based on UPS for bone associated diseases.

关键词： E3 ubiquitin ligase UPS Osteogenesis bone resorption Osteoblast Osteoclast Chondrocyte PROTAC

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NUMB maintains bone mass by promoting degradation of PTEN and GLI1 via ubiquitination in osteoblasts

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bone Research 2018年第4期6卷 368-382页

作者： Ling Ye Feng Lou Fanyuan Yu Demao Zhang Chenglin Wang Fanzi Wu Xin Li Yilin Ping Xiao Yang Jing Yang Dian Chen Bo Gao Dingming Huang Peng Liu State Key laboratory of Oral Disease West China Hospital of Stomatology Sichuan University The Mount Sinai bone Program Department of MedicineMount Sinai School of Medicine

The adaptor protein NUMB is involved in asymmetric division and cell fate determination and recognized as an antagonist of *** studies have proved that Notch activation in osteoblasts contributes to a high bone mass. In this study, however, an osteopenic phenotype was found in 9-week-old mice using osteoblastic specific Col1a1–2.3-Cre to ablate both Numb and its homologue Numbl. The trabecular bone mass decreased dramatically while the cortical bone mass was unaffected. Here, the Notch signal was not activated,while the tensin homologue deleted on human chromosome 10(PTEN), which dephosphorylates phosphatidylinositide 3-kinases, was elevated, attenuating protein kinase B(Akt). The ubiquitination assay revealed that NUMB may physiologically promote PTEN ubiquitination in the presence of neural precursor cell-expressed developmentally downregulated protein 4–1. In addition, the deficiency of Numb/Numbl also activated the Hedgehog pathway through GLI1. This process was found to improve the ratio of the receptor activator of nuclear factor-k B ligand to osteoprotegerin, which enhanced the differentiation of osteoclasts and bone resorption. In conclusion, this study provides an insight into new functons of NUMB and NUMBL on bone homeostasis.

关键词： NUMB maintains bone mass by promoting degradation of PTEN and GLI1 via ubiquitination in osteoblasts GLI RANKL

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