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骨研究：英文

骨研究：英文

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《Bone Research》(骨研究)是由中华人民共和国教育部主管，四川大学主办的骨科学专业英文学术期刊，其组委会由全球顶尖的骨科学专家组成。是中国大陆骨科学研究领域唯一的有国内统一连续出版物号的英文期刊，旨在为全球骨科学研究者搭建一个相互交流的国际性开放平台。
  • 发文量：247
  • 被引量：147
  • H指数：0
  • 开始收录时间：2013,1(1)
  • CNKI综合因子：1.879
  • 维普期刊影响因子： 1.62
  • 万方期刊影响因子：0.96
  • 创刊时间：2013
  • 国内刊号/CN：51-1745/R
    国际刊号/ISSN：2095-4700
  • 发行周期：季刊
    邮发代号：62-272
  • 主管单位：中华人民共和国教育部
    主办单位：四川大学
骨研究：英文-联系信息
  • 主编：周学东
  • 电话：028-85546461
  • 邮箱：br@scu.edu.cn
  • 地址：成都市人民南路三段14号华西口腔医学院编辑部B801
  • 邮编：610041
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骨研究：英文 >2023年第3期

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  • 摘要：Osteoclasts,the bone-resorbing cells,play a pivotal role in skeletal development and adult bone remodeling.They also participate in the pathogenesis of various bone disorders.Osteoclasts differentiate from cells of the monocyte/macrophage lineage upon stimulation of two essential factors,the monocyte/ macrophage colony stimulating factor(M-CSF)and receptor activation of NF-кB ligand(RANKL).M-CSF binds to its receptor c-Fms to activate distinct signaling pathways to stimulate the proliferation and survival of osteoclast precursors and the mature cell.RANKL,however,is the primary osteoclast differentiation factor,and promotes osteoclast differentiation mainly through controlling gene expression by activating its receptor,RANK.Osteoclast function depends on polarization of the cell,induced by integrin αvβ3,to form the resorptive machinery characterized by the attachment to the bone matrix and the formation of the bone-apposed ruffled border.Recent studies have provided new insights into the mechanism of osteoclast differentiation and bone resorption.In particular,c-Fms and RANK signaling have been shown to regulate bone resorption by cross-talking with those activated by integrin αvβ3.This review discusses new advances in the understanding of the mechanisms of osteoclast differentiation and function.
  • 摘要：Bone mineral,adipose tissue and energy metabolism are interconnected by a complex and multilevel series of networks.Calcium and phosphorus are utilized for insulin secretion and synthesis of high energy compounds.Adipose tissue store lipids and cholecalciferol,which,in turn,can influence calcium balance and energy expenditure.Hormones long-thought to solely modulate energy and mineral homeostasis may influence adipocytic function.Osteoblasts are a target of insulin action in bone.Moreover,endocrine mediators,such as osteocalcin,are synthesized in the skeleton but regulate carbohydrate disposal and insulin secretion.Finally,osteoblasts and adipocytes originate from the same mesenchymal progenitor.The mutual crosstalk between osteoblasts and adipocytes within the bone marrow microenvironment plays a crucial role in bone remodeling.In the present review we provide an overview of the reciprocal control between bone and energy metabolism and its clinical implications.
  • 摘要：Survival of children with chronic medical illnesses is leading to an increase in secondary osteoporosis due to impaired peak bone mass(PBM).Insulin-like growth factor type 1(IGF-1) levels correlate with the pattern of bone mass accrual and many chronic illnesses are associated with low IGF-1 levels.Reduced serum levels of IGF-1 minimally affect the integrity of the skeleton,whereas recent studies suggest that skeletal IGF-I regulates PBM.To determine the role of IGF-1 in postnatal bone mass accrual regardless of source,we established an inducible type 1 Igf receptor Cre/lox knockout mouse model,in which the type 1 Igf receptor was deleted inducibely in the mesenchymal stem cells(MSCs) from 3-7 weeks of age.The size of the mouse was not affected as knockout and wild type mice had similar body weights and nasoanal and femoral lengths.However,bone volume and trabecular bone thickness were decreased in the secondary spongiosa of female knockout mice relative to wild type controls,indicating that IGF-1 is critical for bone mass.IGF-1 signaling in MSCs in vitro has been implicated to be involved in both migration to the bone surface and differentiation into bone forming osteoblasts.To clarify the exact role of IGF-1 in bone,we found by immunohistochemical analysis that a similar number of Osterix-positive osteoprogenitors were on the bone perimeter,indicating migration of MSCs was not affected.Most importantly,56% fewer osteocalcin-positive mature osteoblasts were present on the bone perimeter in the secondary spongiosa in knockout mice versus wild type littermates.These in vivo data demonstrate that the primary role of skeletal IGF-1 is for the terminal differentiation of osteoprogenitors,but refute the role of IGF-1 in MSC migration in vivo.Additionally,these findings confirm that impaired IGF-1 signaling in bone MSCs is sufficient to impair bone mass acquisition.
  • 摘要：Current treatment options for skeletal repair,including immobilization,rigid fixation,alloplastic materials and bone grafts,have significant limitations.Bone tissue engineering offers a promising method for the repair of bone deficieny caused by fractures,bone loss and tumors.The use of adipose derived stem cells(ASCs) has received attention because of the self-renewal ability,high proliferative capacity and potential of osteogenic differentiation in vitro and in vivo studies of bone regeneration.Although cell therapies using ASCs are widely promising in various clinical fields,no large human clinical trials exist for bone tissue engineering.The aim of this review is to introduce how they are harvested,examine the characterization of ASCs,to review the mechanisms of osteogenic differentiation,to analyze the effect of mechanical and chemical stimuli on ASC osteodifferentiation,to summarize the current knowledge about usage of ASC in vivo studies and clinical trials,and finally to conclude with a general summary of the field and comments on its future direction.
  • 摘要：Objective:To address the effect of intrinsic factors on craniofacial growth by analyzing the craniofacial morphology of unoperated isolated cleft palate in Chinese adult.Materials and Methods:This study included 37 nonsyndromic isolated cleft palate and 39 age and gender matched non-clefts.Twenty-six cephalometric measurements were employed to evaluate the facial morphology.Independent samples T test and Mann-Whitney U were used for comparison.Significant difference was defined at 95% level.Results:Data from this study showed patients with unoperated isolated cleft palate have a reduced maxillary sagittal length(ANS-PMP,A-PMP,P0.05),depth of bony pharynx(Ba-PMP,P>0.05),anterior and posterior maxillary height(N-ANS,P>0.05;R-PMP,P>0.05) and mandible morphology(including linear measurements and angle measurements) did not show any significant difference between case and control groups.Conclusions:Patients with isolated cleft palate were characterized by maxillary retrusion.Mandible morphology and cranial basal morphology in isolated cleft palate showed no significant difference with nonclefts.Patients with isolated cleft palate are more vulnerable to cross bite than nonclefts.Intrinsic deficiencies did detrimental effect on maxilla sagittal length,but did no detrimental effect on maxilla position,mandible size and position.
  • 摘要：Online submission and review system at http://mcO3.manuscriptcentral.com/brBone Research is supported byWest China School of Stomatology,Sichuan University State Key Laboratory of Oral Diseases,Sichuan University International Chinese Hard Tissue Society (ICHTS)
  • 摘要：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.
  • 摘要：A decade ago,only two hormones,parathyroid hormone and 1,25(OH)2D,were widely recognized to direct-ly affect phosphate homeostasis.Since the discovery of fibroblast growth factor 23(FGF23) in 2000(1),our understanding of the mechanisms of phosphate homeostasis and of bone mineralization has grown exponentially.FGF23 is the link between intestine,bone,and kidney together in phosphate regulation.However,we still do not know the complex mechanism of phosphate homeostasis and bone mineralization.The physiological role of FGF23 is to regulate serum phosphate.Secreted mainly by osteocytes and osteo-blasts in the skeleton(2-3),it modulates kidney handling of phosphate reabsorption and calcitriol produc-tion.Genetic and acquired abnormalities in FGF23 structure and metabolism cause conditions of either hyper-FGF23 or hypo-FGF23.Hyper-FGF23 is related to hypophosphatemia,while hypo-FGF23 is related to hyperphosphatemia.Both hyper-FGF23 and hypo-FGF23 are detrimentalto humans.In this review,we will discuss the pathophysiology of FGF23 and hyper-FGF23 related renal phosphate wasting disorders(4).
  • 摘要：The importance of the thyroid hormone axis in the regulation of skeletal growth and maintenance has been well established from clinical studies involving patients with mutations in proteins that regulate synthesis and/or actions of thyroid hormone.Data from genetic mouse models involving disruption and overexpression of components of the thyroid hormone axis also provide direct support for a key role for thyroid hormone in the regulation of bone metabolism.Thyroid hormone regulates proliferation and/or differentiated actions of multiple cell types in bone including chondrocytes,osteoblasts and osteoclasts.Thyroid hormone effects on the target cells are mediated via ligand-inducible nuclear receptors/transcription factors,thyroid hormone receptor(TR) α and β,of which TRα seems to be critically important in regulating bone cell functions.In terms of mechanisms for thyroid hormone action,studies suggest that thyroid hormone regulates a number of key growth factor signaling pathways including insulin-like growth factor-I,parathyroid hormone related protein,fibroblast growth factor,Indian hedgehog and Wnt to influence skeletal growth.In this review we describe findings from various genetic mouse models and clinical mutations of thyroid hormone signaling related mutations in humans that pertain to the role and mechanism of action of thyroid hormone in the regulation of skeletal growth and maintenance.
  • 摘要：In the 1970s,with the advent of biochemical multichannel screening in the United States and other western countries,the clinical presentation of primary hyperparathyroidism(PHPT) changed from a symptomatic to an asymptomatic disorder.However,in Asian countries,like China,PHPT did not show this evolution,but rather continued to be a symptomatic disease with target organ involvement.In this paper,we revisit the clinical features of PHPT in New York and Shanghai,representative United States and Chinese cites,over the past decade.The questions we address are whether the disease evolved in China to a more asymptomatic one and,whether in the United States further changes are evident.The results indicate that while PHPT con-tinues to present primarily as an asymptomatic disease in the United States,a new phenotype characterized by normal serum calcium and high parathyroid hormone levels,normocalcemic PHPT,has emerged.Data from Shanghai demonstrates a trend for PHPT to present more commonly as an asymptomatic disorder in China.However,most patients with PHPT in China still manifest classical symptoms,i.e.nephrolithiasis and fractures.A comparison of the two cohorts shows that Chinese patients with PHPT are younger,with higher serum calcium and PTH levels,and lower 25-hydroxyvitamin D levels than patients in New York.Normocalcemic PHPT has not yet been recognized in Shanghai.In summary,although the phenotypes of PHPT in both cities are evolving towards less evident disease,sharp clinical and biochemical differences are still apparent in PHPT as expressed in China and the United States.
  • 摘要：Apical periodontitis,dominated by dense inflammatory infiltrates and increased osteoclast activities,can lead to alveolar bone destruction and tooth loss.It is believed that miRNA participates in regulating various biological processes,osteoclastogenesis included.This study aims to investigate the differential expression of miRNAs in rat apical periodontitis and explore their functional target genes.Microarray analysis was used to identify differentially expressed miRNAs in apical periodontitis.Bioinformatics technique was applied for predicting the target genes of differentially expressed miRNAs and their biological functions.The result provided us with an insight into the potential biological effects of the differentially expressed miRNAs and showed particular enrichment of target genes involved in the MAPK signaling pathways.These findings may highlight the intricate and specific roles of miRNA in inflammation and osteoclastogenesis,both of which are key aspects of apical periodontitis,thus contributing to the future investigation into the etiology,under-lying mechanism and treatment of apical periodontitis.
  • 摘要：The role of Bone Tissue Engineering in the field of Regenerative Medicine has been the topic of substantial research over the past two decades.Technological advances have improved orthopaedic implants and surgical techniques for bone reconstruction.However,improvements in surgical techniques to reconstruct bone have been limited by the paucity of autologous materials available and donor site morbidity.Recent advances in the development of biomaterials have provided attractive alternatives to bone grafting expanding the surgical options for restoring the form and function of injured bone.Specifically,novel bioactive(second generation)biomaterials have been developed that are characterised by controlled action and reaction to the host tissue environment,whilst exhibiting controlled chemical breakdown and resorption with an ultimate replacement by regenerating tissue.Future generations of biomaterials(third generation)are designed to be not only osteoconductive but also osteoinductive,i.e.to stimulate regeneration of host tissues by combining tissue engineering and in situ tissue regeneration methods with a focus on novel applications.These techniques will lead to novel possibilities for tissue regeneration and repair.At present,tissue engineered constructs that may find future use as bone grafts for complex skeletal defects,whether from post-traumatic,degenerative,neoplastic or congenital/developmental"origin"require osseous reconstruction to ensure structural and functional integrity.Engineering functional bone using combinations of cells,scaffolds and bioactive factors is a promising strategy and a particular feature for future development in the area of hybrid materials which are able to exhibit suitable biomimetic and mechanical properties.This review will discuss the state of the art in this field and what we can expect from future generations of bone regeneration concepts.
  • 摘要：Insulin-like growth factor-I(IGF-I)regulates cell growth,survival,and differentiation by acting on the IGF-I receptor,(IGF-IR)-a tyrosine kinase receptor,which elicits diverse intracellular signaling responses.All skeletal cells express IGF-I and IGF-IR.Recent studies using tissue/cell-specific gene knockout mouse models and cell culture techniques have clearly demonstrated that locally produced IGF-I is more critical than the systemic IGF-I in supporting embryonic and postnatal skeletal development and bone remodeling.Local IGF-I/IGF-IR signaling promotes the growth,survival and differentiation of chondrocytes and osteoblasts,directly and indirectly,by altering other autocrine/paracrine signaling pathways in cartilage and bone,and by enhancing interactions among these skeletal cells through hormonal and physical means.Moreover,local IGF-I/IGF-IR signaling is critical for the anabolic bone actions of growth hormone and parathyroid hormone.Herein,we review evidence supporting the actions of local IGF-I/IGF-IR in the above aspects of skeletal development and remodeling.
  • 摘要：Mechanical forces play critical roles in the development and remodeling processes of bone.As an alternative cell source for bone engineering,adipose-derived stem cells(ASCs)should be fully investigated for their responses to mechanical stress.Similarly,the osteogenic potential,stimulated by mechanical stress,should be compared with bone marrow stromal cells(BMSCs),which have been clinically used for bone tissue engineering.In this study,ASCs and BMSCs were osteogenic-induced for 48 hours,and then subjected to uniaxial mechanical stretching for 2 or 6 hours.Cell orientation,osteogenic regulatory genes,osteogenic genes and ALP activities were measured and compared between ASCs and BMSCs.ASCs could align in a perpendicular way to the direction of stretching stress,while BMSCs did not present a specific alignment.Both 2 and 6 hours mechanical stretching could enhance the mRNA expression of Osx and Runx2 in BMSCs and ASCs,while OCN mRNA only increased in ASCs after 6 hours mechanical loading.Mechanical stretching enhanced the BMP-2 mRNA expression in ASCs,while only after 6 hours of mechanical loading significantly increased the BMP-2 gene expression in BMSCs.Significant differences only exist between ASCs and BMSCs loaded at 2 hours of mechanical stretching.It is concluded that ASCs are more rapid responders to mechanical stress,and have greater potential than BMSCs in osteogenesis when stimulated by mechanical stretching,indicating their usefulness for bone study in a rat model.
  • 摘要：Little is known about early coincidental changes in bone and vascular properties,particularly in the context of skeletal anabolism(puberty)versus relative equilibrium(young adulthood).We aimed to determine if subclinical markers of vascular function were associated with bone mineral content(BMC)and to evaluate the contribution of systemic factors in healthy females ages 14-42 years.Endothelial function was assessed by flow mediated dilatation(FMD),arterial stiffness by pulse wave velocity(PWV)and augmentation index(AIx),blood pressure(BP)by sphygmomanometer,BMC by DXA,and systemic factors by fasting blood draw.General linear models controlled for age,race and height indicated a positive association between systolic BP(SBP)and BMC independent of systemic factors.When stratified by age using 19 years as a cut-point,there was an inverse relationship between AIx75 in adolescents with insulin(P<0.10)or inflammatory markers(P<0.10)in statistical models.Conversely,there was a positive relationship between BMC and both PWV and AIx75 in young adults(P<0.05).The link between bone and the vasculature may be life stage-dependent.In the context of a less dynamic microenvironment in young adult females,metabolic factors appear to moderate less of an effect of hemodynamic properties on the skeleton relative to adolescents.
  • 摘要：Bone Mineral Density(BMD)is a gold standard for the diagnosis of osteoporosis and is also important in the assessment of fracture risk.Other risk factors have been identified that together make up fracture risk assessment tools such as FRAX.Another potential factor,circulating lipids,has been suggested because of reports linking statins to fracture risk reduction.We analyzed the lipid profile in a cohort of women diagnosed with postmenopausal osteoporosis based on bone density determination:610 women with osteoporosis(mean lumbar spine T-score-3.16±0.81,mean yrs.since menopause 15.79±8.9)were grouped according to age at evaluation(70 years),the presence/absence of a history of a fragility fracture,statin and/or antiresorptive drug use.There was no correlation between BMD and Body Mass Index(BMI:P>0.05,r2<0.02).However,when BMD was correlated with both BMI and the lipid profile(Triglycerides,Cholesterol,LDLc,HDLc),significant correlations were found in 5 cohorts:51-60 years with fractures(n=61,r2=0.14,P<0.01),61-70 years(n=201,r2=0.09,P<0.01)with fractures(n=88,r2=0.14,P<0.01)or without fractures(n=113,r2=0.24,P=0.02)and over 70 years(n=247,r2=0.11,P<0.01).
  • 摘要：The importance of the vascular supply for bone is well-known to orthopaedists but is still rather overlooked within the wider field of skeletal research.Blood supplies oxygen,nutrients and regulatory factors to tissues,as well as removing metabolic waste products such as carbon dioxide and acid.Bone receives up to about 10% of cardiac output,and this blood supply permits a much higher degree of cellularity,remodelling and repair than is possible in cartilage,which is avascular.The blood supply to bone is delivered to the endosteal cavity by nutrient arteries,then flows through marrow sinusoids before exiting via numerous small vessels that ramify through the cortex.The marrow cavity affords a range of vascular niches that are thought to regulate the growth and differentiation of hematopoietic and stromal cells,in part via gradients of oxygen tension.The quality of vascular supply to bone tends to decline with age and may be compromised in common pathological settings,including diabetes,anaemias,chronic airway diseases and immobility,as well as by tumours.Reductions in vascular supply are associated with bone loss.This may be due in part to the direct effects of hypoxia,which blocks osteoblast function and bone formation but causes reciprocal increases in osteoclastogenesis and bone resorption.Common regulatory factors such as parathyroid hormone or nitrates,both of which are potent vasodilators,might exert their osteogenic effects on bone via the vasculature.These observations suggest that the bone vasculature will be a fruitful area for future research.
  • 摘要：Regulator of G-protein Signaling 10(Rgs10)plays an important function in osteoclast differentiation.However,the role of Rgs10 in immune cells and inflammatory responses,which activate osteoclasts in inflammatory lesions,such as bacteria-induced periodontal disease lesions,remains largely unknown.In this study,we used an adeno-associated virus(AAV-)mediated RNAi(AAV-shRNA-Rgs10)knockdown approach to study Rgs10’s function in immune cells and osteoclasts in bacteria-induced inflammatory lesions in a mouse model of periodontal disease.We found that AAV-shRNA-Rgs10 mediated Rgs10 knockdown impaired osteoclastogenesis and osteoclast-mediated bone resorption,in vitro and in vivo.Interestingly,local injection of AAV-shRNA-Rgs10 into the periodontal tissues in the bacteria-induced inflammatory lesion greatly decreased the number of dendritic cells,T-cells and osteoclasts,and protected the periodontal tissues from local inflammatory damage and bone destruction.Importantly,AAV-mediated Rgs10 knockdown also reduced local expression of osteoclast markers and pro-inflammatory cytokines.Our results demonstrate that AAVshRNA-Rgs10 knockdown in periodontal disease tissues can prevent bone resorption and inflammation simultaneously.Our data indicate that Rgs10 may regulate dendritic cell proliferation and maturation,as well as the subsequent stimulation of T-cell proliferation and maturation,and osteoclast differentiation and activation.Our study suggests that AAV-shRNA-Rgs10 can be useful as a therapeutic treatment of periodontal disease.
  • 摘要：Bone Research is supported by West China School of Stomatology,Sichuan University State Key Laboratory of Oral Diseases,Sichuan University International Chinese Hard Tissue Society(ICHTS)Type of manuscript accepted Review articles provide a comprehensive review of the state of the art on topics selected by the Editor-in-Chief.Reviews should not be submitted without contacting the Editorial Office.The word limit is10 000
  • 摘要：NF-κBp50/p52 double knockout(dKO)and RANK KO mice have no osteoclasts and develop severe osteopetrosis associated with dwarfism.In contrast,Op/Op mice,which form few osteoclasts,and Src KO mice,which have osteoclasts with defective resorptive function,are osteopetrotic,but they are not dwarfed.Here,we compared the morphologic features of long bones from p50/p52 dKO,RANK KO,Op/Op and Src KO mice to attempt to explain the differences in their long bone lengths.We found that growth plates in p50/p52 dKO and RANK KO mice are significantly thicker than those in WT mice due to a 2-3-fold increase in the hypertrophic chondrocyte zone associated with normal a proliferative chondrocyte zone.This growth plate abnormality disappears when animals become older,but their dwarfism persists.Op/Op or Src KO mice have relatively normal growth plate morphology.In-situ hybridization study of long bones from p50/p52 dKO mice showed marked thickening of the growth plate region containing type 10 collagen-expressing chondrocytes.Treatment of micro-mass chondrocyte cultures with RANKL did not affect expression levels of type 2 collagen and Sox9,markers for proliferative chondrocytes,but RANKL reduced the number of type 10collagen-expressing hypertrophic chondrocytes.Thus,RANK/NF-κB signaling plays a regulatory role in post-natal endochondral ossification that maintains hypertrophic conversion and prevents dwarfism in normal mice.
  • 摘要：Recent improvements in the speed and accuracy of DNA sequencing,together with increasingly sophisticated mathematical approaches for annotating gene networks,have revolutionized the field of human genetics and made these once time consuming approaches assessable to most investigators.In the field of bone research,a particularly active area of gene discovery has occurred in patients with rare bone disorders such as osteogenesis imperfecta(OI)that are caused by mutations in single genes.In this perspective,we highlight some of these technological advances and describe how they have been used to identify the genetic determinants underlying two previously unexplained cases of OI.The widespread availability of advanced methods for DNA sequencing and bioinformatics analysis can be expected to greatly facilitate identification of novel gene networks that normally function to control bone formation and maintenance.
  • 摘要：Osteoporotic hip fracture is associated with significant trabecular bone loss,which is typically characterized as low bone density by dual-energy X-ray absorptiometry(DXA)and altered microstructure by micro-computed tomography(μCT).Emerging morphological analysis techniques,e.g.individual trabecula segmentation(ITS),can provide additional insights into changes in plate-like and rod-like trabeculae,two major micro-structural types serving different roles in determining bone strength.Using ITS,we evaluated trabecular microstructure of intertrochanteric bone cores obtained from 23 patients undergoing hip replacement surgery for intertrochanteric fracture and 22 cadaveric controls.Micro-finite element(μFE)analyses were performed to further understand how the abnormalities seen by ITS might translate into effects on bone strength.ITS analyses revealed that,near fracture site,plate-like trabeculae were seriously depleted in fracture patients,but trabecular rod volume was maintained.Besides,decreased plate area and rod length were observed in fracture patients.Fracture patients also showed decreased elastic moduli and shear moduli of trabecular bone.These results provided evidence that in intertrochanteric hip fracture,preferential loss of plate-like trabeculae led to more rod-like microstructure and deteriorated mechanical competence adjacent to the fracture site,which increased our understanding of the biomechanical pathogenesis of hip fracture in osteoporosis.
  • 摘要：Objective:The aim of this study was to investigate the effects of plumbagin(PL),a naphthoquinone derived from the medicinal plant plumbago zeylanica,on the invasion and migration of human breast cancer cells.Methods:Human breast cancer MDA-MB-231SArfp cells were treated with different concentrations of plumbagin for 24 h.The effects of plumbagin on the migration and invasion were observed by a transwell method.The expressions of IL-1α,IL-1β,IL-6,IL-8,TGF-β,TNFα,MMP-2 and MMP-9 mRNA in MDA-MB-231SArfp cells were detected using Real-Time PCR.MDA-MB-231SArfp cells were treated with plumbagin at different concentrations for 45 minutes.The activation of STAT3 was detected by western blot.Following this analysis,STAT3 in MDA-MB-231SArfp cells was knocked out using specific siRNA.mRNA levels of IL-1α,TGF-β,MMP-2 and MMP-9 were then detected.Consequently,MDA-MB-231SArfp cells were injected intracardially into BALB/c nude mice to construct a breast cancer bone metastatic model.The mice were injected intraperitoneally with plumbagin.Non-invasive in vivo monitoring,X-ray imaging and histological staining were performed to investigate the effects of plumbagin on the invasion and migration of breast cancer cells in vivo.Results:The in vitro results showed that plumbagin could suppress the migration and invasion of breast cancer cells and down-regulate mRNA expressions of IL-1α,TGF-β,MMP-2 and MMP-9.Western blotting demonstrated that plumbagin inhibited the activation of STAT3 signaling in MDA-MB-231SArfp cells.The inactivation of STAT3 was found to have an inhibitory effect on the expressions of IL-1α,TGF-β,MMP-2 and MMP-9.In vivo studies showed that plumbagin inhibited the metastasis of breast cancer cells and decreased osteolytic bone metastases,as well as the secretion of MMP-2 and MMP-9 by tumor cells at metastatic lesions.Conclusions:Plumbagin can suppress the invasion and migration of breast cancer cells via the inhibition of STAT3 signaling and by downregulation of IL-1α,TGF-β,MMP-2 and MMP-9.
  • 摘要：Online submission and review system at http://mc03.manuscriptcentral.com/brBone Research is supported by West China School of Stomatology,Sichuan University State Key Laboratory of Oral Diseases,Sichuan University International Chinese Hard Tissue Society(ICHTS)Type of manuscript accepted Review articles provide a comprehensive review of the state of the art on topics selected by the Editor-in-Chief.Reviews should not be submitted without contacting the Editorial Office.The word limit is10 000 words(not including the title,author affiliations,abstracts。
  • 摘要：Elevated oxidative stress(OS)during aging leads to bone loss.OS increases intracellular Ca2+([Ca2+]i),resulting in cellular damage and death.We show earlier that Cx43 hemichannels open in response to OS,which serves as a protective mechanism for osteocytes.However,the underlying mechanism is unknown.Here,we found that treatment with H2O2increased[Ca2+]i in osteocytes with[Ca2+]i being primarily derived from an extracellular Ca2+source.Hemichannel opening induced by OS was inhibited by the depletion of[Ca2+]i with BAPTA-AM,a Ca2+chelator,suggesting that[Ca2+]i influenced the activity of Cx43 hemichannels.Conversely,blockade of hemichannels had no effect on[Ca2+]i.A biotinylation assay showed that cell surface-expressed Cx43 was increased by OS,which could be inhibited by BAPTA-AM,suggesting that[Ca2+]i is necessary for Cx43 migration to the cell surface in response to OS.Together,these data suggest that increased hemichannel activity induced by OS was likely to be caused by elevated[Ca2+]i through increased Cx43 on the cell surface.
  • 摘要：Bone is a highly vascularized tissue,although this aspect of bone is often overlooked.In this article,the importance of blood flow in bone repair and regeneration will be reviewed.First,the skeletal vascular anatomy,with an emphasis on long bones,the distinct mechanisms for vascularizing bone tissue,and methods for remodeling existing vasculature are discussed.Next,techniques for quantifying bone blood flow are briefly summarized.Finally,the body of experimental work that demonstrates the role of bone blood flow in fracture healing,distraction osteogenesis,osteoporosis,disuse osteopenia,and bone grafting is examined.These results illustrate that adequate bone blood flow is an important clinical consideration,particularly during bone regeneration and in at-risk patient groups.
  • 摘要：Induced pluripotent stem cells(iPSCs)have great potential due to their proliferation and differentiation capability.The objectives of this study were to generate iPSC-derived mesenchymal stem cells(iPSC-MSCs),and investigate iPSC-MSC proliferation and osteogenic differentiation on calcium phosphate cement(CPC)containing biofunctional agents for the first time.Human iPSCs were derived from marrow CD34+cells which were reprogrammed by a single episomal vector.iPSCs were cultured to form embryoid bodies(EBs),and MSCs migrated out of EBs.Five biofunctional agents were incorporated into CPC:RGD(Arg-Gly-Asp)peptides,fibronectin(Fn),fibronectin-like engineered polymer protein(FEPP),extracellular matrix Geltrex,and platelet concentrate.iPSC-MSCs were seeded on five biofunctionalized CPCs:CPC-RGD,CPC-Fn,CPC-FEPP,CPC-Geltrex,and CPC-Platelets.iPSC-MSCs on biofunctional CPCs had enhanced proliferation,actin fiber expression,osteogenic differentiation and mineralization,compared to control.Cell proliferation was greatly increased on biofunctional CPCs.iPSC-MSCs underwent osteogenic differentiation with increased alkaline phosphatase,Runx2 and collagen-I expressions.Mineral synthesis by iPSC-MSCs on CPC-Platelets was 3-fold that of CPC control.In conclusion,iPSCs showed high potential for bone engineering.iPSC-MSCs on biofunctionalized CPCs had cell proliferation and bone mineralization that were much better than traditional CPC.iPSC-MSC-CPC constructs are promising to promote bone regeneration in craniofacial/orthopedic repairs.
  • 摘要：A number of effective therapies for the treatment of osteoporosis have become available in recent years.However,uncertainty exists regarding their long-term use and effectiveness.Bisphosphonate treatment,unlike hormone replacement,denosumab or teriparatide,is associated with benefits extended even after treatment discontinuation.The extended benefits are most apparent for alendronate(ALN)and zoledronate(ZOL).A drug holiday might be considered in patients at low-moderate risk and who have been fully compliant with treatment,and who have had a response to treatment.In patients at low-moderate risk of fractures the decision to consider a drug holiday should be balanced also with the safety profile of each treatment.
  • 摘要：TGF-β1–3 are unique multi-functional growth factors that are only expressed in mammals,and mainly secreted and stored as a latent complex in the extracellular matrix(ECM).The biological functions of TGF-βin adults can only be delivered after ligand activation,mostly in response to environmental perturbations.Although involved in multiple biological and pathological processes of the human body,the exact roles of TGF-βin maintaining stem cells and tissue homeostasis have not been well-documented until recent advances,which delineate their functions in a given context.Our recent findings,along with data reported by others,have clearly shown that temporal and spatial activation of TGF-βis involved in the recruitment of stem/progenitor cell participation in tissue regeneration/remodeling process,whereas sustained abnormalities in TGF-βligand activation,regardless of genetic or environmental origin,will inevitably disrupt the normal physiology and lead to pathobiology of major diseases.Modulation of TGF-βsignaling with different approaches has proven effective pre-clinically in the treatment of multiple pathologies such as sclerosis/fibrosis,tumor metastasis,osteoarthritis,and immune disorders.Thus,further elucidation of the mechanisms by which TGF-βis activated in different tissues/organs and how targeted cells respond in a context-dependent way can likely be translated with clinical benefits in the management of a broad range of diseases with the involvement of TGF-β.
  • 摘要：The mammalian/mechanistic target of rapamycin(mTOR)is a serine/threonine protein kinase that integrates inputs from nutrients and growth factors to control many fundamental cellular processes through two distinct protein complexes mTORC1 and mTORC2.Recent mouse genetic studies have established that mTOR pathways play important roles in regulating multiple aspects of skeletal development and homeostasis.In addition,mTORC1 has emerged as a common effector mediating the bone anabolic effect of Igf1,Wnt and Bmp.Dysregulation of mTORC1 could contribute to various skeletal diseases including osteoarthritis and osteoporosis.Here we review the current understanding of mTOR signaling in skeletal development and bone homeostasis,as well as in the maintenance of articular cartilage.We speculate that targeting mTOR signaling may be a valuable approach for treating skeletal diseases.

    骨研究：英文的期刊信息

    • 创刊时间：2013
    • 地区：CHINA MAINLAND
    • 语言：中文
    • 热门主题：BONE SUBMISSION INFORMATION HOMEOSTASIS OSTEOARTHRITIS SKELETAL OSTEOPOROSIS OSTEOBLASTS OSTEOBLAST 成骨细胞分化
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      1

      CELL & TISSUE ENGINEERING:Q1;

      Biochemistry, Genetics and Molecular Biology:Physiology;Medicine:Endocrinology, Diabetes and Metabolism;Histology;

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