BoneKEy reports最新文献_第10页

Bone remodeling markers and bone metastases: From cancer research to clinical implications. 骨重塑标志物和骨转移:从癌症研究到临床意义。

BoneKEy reports Pub Date : 2015-04-22 eCollection Date: 2015-01-01 DOI: 10.1038/bonekey.2015.35

Arlindo Ferreira, Irina Alho, Sandra Casimiro, Luís Costa

引用次数: 46

Bone marrow stroma-derived miRNAs as regulators, biomarkers and therapeutic targets of bone metastasis. 骨髓基质衍生的 miRNA 是骨转移的调节因子、生物标志物和治疗靶标。

BoneKEy reports Pub Date : 2015-04-15 eCollection Date: 2015-01-01 DOI: 10.1038/bonekey.2015.38

Maša Alečković, Yibin Kang

{"title":"Bone marrow stroma-derived miRNAs as regulators, biomarkers and therapeutic targets of bone metastasis.","authors":"Maša Alečković, Yibin Kang","doi":"10.1038/bonekey.2015.38","DOIUrl":"10.1038/bonekey.2015.38","url":null,"abstract":"MicroRNAs (miRNAs) are short, endogenous RNA molecules that have essential roles in regulating gene expression. They control numerous physiological and cellular processes, including normal bone organogenesis and homeostasis, by enhancing or inhibiting bone marrow cell growth, differentiation, functional activity and crosstalk of the multiple cell types within the bone. Hence, elucidating miRNA targets in bone marrow stromal cells has revealed novel regulations during bone development and maintenance. Moreover, recent studies have detailed the capacity for bone stromal miRNAs to influence bone metastasis from a number of primary carcinomas by interfering with bone homeostasis or by directly influencing metastatic tumor cells. Owing to the current lack of good diagnostic biomarkers of bone metastases, such changes in bone stromal miRNA expression in the presence of metastatic lesions may become useful biomarkers, and may even serve as therapeutic targets. In particular, cell-free and exosomal miRNAs shed from bone stromal cells into circulation may be developed into novel biomarkers that can be routinely measured in easily accessible samples. Taken together, these findings reveal the significant role of bone marrow stroma-derived miRNAs in the regulation of bone homeostasis and bone metastasis. ","PeriodicalId":72441,"journal":{"name":"BoneKEy reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4398005/pdf/bonekey201538.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33247661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Bone specific immunity and its impact on metastasis. 骨特异性免疫及其对转移的影响。

BoneKEy reports Pub Date : 2015-04-15 eCollection Date: 2015-01-01 DOI: 10.1038/bonekey.2015.32

Nikola Baschuk, Jay Rautela, Belinda S Parker

{"title":"Bone specific immunity and its impact on metastasis.","authors":"Nikola Baschuk, Jay Rautela, Belinda S Parker","doi":"10.1038/bonekey.2015.32","DOIUrl":"https://doi.org/10.1038/bonekey.2015.32","url":null,"abstract":"Bone is one of the most common sites of metastasis in solid malignancy. Contributing to this osteotropism are the dynamic interactions between tumor cells and the numerous cell types resident in the normal bone, particularly osteoclasts and osteoblasts, which create a tumor supporting microenvironment. However, disseminated cells are detected in the bone marrow long before evidence of metastatic outgrowth, and it is likely that prolonged survival is also reliant on immunoescape. Compared with other peripheral organs such as the lung and spleen, the bone marrow constitutes a unique immune cell compartment that likely provides an immune privileged niche for disseminated tumor cells. This includes the large proportions of immunosuppressive cells, including myeloid derived suppressor cells and regulatory T cells, that blunt the activity of cytotoxic lymphocytes involved in tumor immunosurveillance. This review highlights key aspects of the osteoimmune landscape and emerging mechanisms by which tumor cells create or co-opt an immunosuppressed niche to support their outgrowth in bone. Future studies in this field are likely to shed light on the differences in immunoregulation between the bone and other sites including the primary tumor, and the potential for immunotherapeutics in treating disseminated disease in the bone. However, more immunocompetent models, that recapitulate tumor heterogeneity and bone metastasis need to be developed to accelerate this field. ","PeriodicalId":72441,"journal":{"name":"BoneKEy reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1038/bonekey.2015.32","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33247659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 41

Assessment of bone vascularization and its role in bone remodeling. 评估骨血管化及其在骨重塑中的作用。

BoneKEy reports Pub Date : 2015-04-08 eCollection Date: 2015-01-01 DOI: 10.1038/bonekey.2015.29

Marie-Hélène Lafage-Proust, Bernard Roche, Max Langer, Damien Cleret, Arnaud Vanden Bossche, Thomas Olivier, Laurence Vico

引用次数: 111

Role of syndecan-2 in osteoblast biology and pathology. syndecan-2在成骨细胞生物学和病理学中的作用。

BoneKEy reports Pub Date : 2015-04-01 eCollection Date: 2015-01-01 DOI: 10.1038/bonekey.2015.33

Rafik Mansouri, Eric Haÿ, Pierre J Marie, Dominique Modrowski

引用次数: 21

Molecular alterations that drive breast cancer metastasis to bone. 导致乳腺癌骨转移的分子改变。

BoneKEy reports Pub Date : 2015-03-18 eCollection Date: 2015-01-01 DOI: 10.1038/bonekey.2015.10

Penelope D Ottewell, Liam O'Donnell, Ingunn Holen

{"title":"Molecular alterations that drive breast cancer metastasis to bone.","authors":"Penelope D Ottewell, Liam O'Donnell, Ingunn Holen","doi":"10.1038/bonekey.2015.10","DOIUrl":"https://doi.org/10.1038/bonekey.2015.10","url":null,"abstract":"Epithelial cancers including breast and prostate commonly progress to form incurable bone metastases. For this to occur, cancer cells must adapt their phenotype and behaviour to enable detachment from the primary tumour, invasion into the vasculature, and homing to and subsequent colonisation of bone. It is widely accepted that the metastatic process is driven by the transformation of cancer cells from a sessile epithelial to a motile mesenchymal phenotype through epithelial-mesenchymal transition (EMT). Dissemination of these motile cells into the circulation provides the conduit for cells to metastasise to distant organs. However, accumulating evidence suggests that EMT is not sufficient for metastasis to occur and that specific tissue-homing factors are required for tumour cells to lodge and grow in bone. Once tumour cells are disseminated in the bone environment, they can revert into an epithelial phenotype through the reverse process of mesenchymal-epithelial transition (MET) and form secondary tumours. In this review, we describe the molecular alterations undertaken by breast cancer cells at each stage of the metastatic cascade and discuss how these changes facilitate bone metastasis. ","PeriodicalId":72441,"journal":{"name":"BoneKEy reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1038/bonekey.2015.10","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33194628","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 35

Bone microdamage, remodeling and bone fragility: how much damage is too much damage? 骨微损伤、骨重塑与骨脆性:多大程度的损伤才算过度损伤?

BoneKEy reports Pub Date : 2015-03-18 eCollection Date: 2015-01-01 DOI: 10.1038/bonekey.2015.11

Zeynep Seref-Ferlengez, Oran D Kennedy, Mitchell B Schaffler

{"title":"Bone microdamage, remodeling and bone fragility: how much damage is too much damage?","authors":"Zeynep Seref-Ferlengez, Oran D Kennedy, Mitchell B Schaffler","doi":"10.1038/bonekey.2015.11","DOIUrl":"https://doi.org/10.1038/bonekey.2015.11","url":null,"abstract":"Microdamage resulting from fatigue or 'wear and tear' loading contributes to bone fragility; however, the full extent of its influence is not completely understood. Linear microcracks (∼50-100 μm) and diffuse damage (clusters of sublamellar-sized cracks) are the two major bone microdamage types, each with different mechanical and biological consequences. Healthy bone, due to its numerous microstructural interfaces and its ability to affect matrix level repair, deals effectively with microdamage. From a material standpoint, healthy bone behaves much like engineering composites like carbon-fiber reinforced plastics. Both materials allow matrix damage to form during fatigue loading and use microstructural interfaces to dissipate energy and limit microcrack propagation to slow fracture. The terms fracture toughness and 'toughening mechanism', respectively, describe mechanical behavior and microstructural features that prevent crack growth and make it harder to fracture a material. Critically, toughness is independent of strength. In bone, primary toughening features include mineral and collagen interfaces, lamellae and tissue heterogeneity among osteons. The damage tolerance of bone and other composites can be overcome with sustained loading and/or matrix changes such that the microstructure no longer limits microcrack propagation. With reduced remodeling due to aging, disease or remodeling suppression, microdamage accumulation can occur along with loss of tissue heterogeneity. Both contribute additively to reduced fracture toughness. Thus, the answer to the key question for bone fragility of how much microdamage is too much is extremely complex. It ultimately depends on the interplay between matrix damage content, internal repair and effectiveness of matrix-toughening mechanisms. ","PeriodicalId":72441,"journal":{"name":"BoneKEy reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1038/bonekey.2015.11","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33194629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 102

Exercise prevents β-aminopropionitrile-induced morphological changes to type I collagen in murine bone. 运动可防止β-氨基丙腈诱导的小鼠骨I型胶原的形态学改变。

BoneKEy reports Pub Date : 2015-03-11 eCollection Date: 2015-01-01 DOI: 10.1038/bonekey.2015.12

Max A Hammond, Joseph M Wallace

{"title":"Exercise prevents β-aminopropionitrile-induced morphological changes to type I collagen in murine bone.","authors":"Max A Hammond, Joseph M Wallace","doi":"10.1038/bonekey.2015.12","DOIUrl":"https://doi.org/10.1038/bonekey.2015.12","url":null,"abstract":"This study evaluated the effects of reduced enzymatic crosslinking, exercise and the ability of exercise to prevent the deleterious impact of reduced crosslinking on collagen D-spacing. Eight-week-old female mice were divided into four weight-matched groups receiving daily injections of either phosphate-buffered saline (PBS) or 300 mg kg(-1) β-aminopropionitrile (BAPN) while undergoing normal cage activity (Sed) or 30 min per day of treadmill exercise (Ex) for 21 consecutive days. BAPN caused a downward shift in the D-spacing distribution in Sed BAPN compared with Sed PBS (P<0.001) but not in Ex BAPN (P=0.429), indicating that exercise can prevent changes in collagen morphology caused by BAPN. Exercise had no effect on D-spacing in PBS control mice (P=0.726), which suggests that exercise-induced increases in lysyl oxidase may be a possible mechanism for preventing BAPN-induced changes in D-spacing. The D-spacing changes were accompanied by an increase in mineral crystallinity/maturity due to the main effect of BAPN (P=0.016). However, no changes in nanoindentation, reference point indentation or other Raman spectroscopy parameters were observed. The ability of exercise to rescue BAPN-driven changes in collagen morphology necessitates further research into the use of mechanical stimulation as a preventative therapy for collagen-based diseases. ","PeriodicalId":72441,"journal":{"name":"BoneKEy reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2015-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1038/bonekey.2015.12","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33152067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 21

Chondrodysplasias and TGFβ signaling. 软骨发育不良和TGFβ信号传导。

BoneKEy reports Pub Date : 2015-03-11 eCollection Date: 2015-01-01 DOI: 10.1038/bonekey.2015.9

Carine Le Goff, Valerie Cormier-Daire

引用次数: 6

HIV infection and osteoporosis. 艾滋病毒感染与骨质疏松症

BoneKEy reports Pub Date : 2015-02-11 eCollection Date: 2015-01-01 DOI: 10.1038/bonekey.2015.3

Juliet Compston

引用次数: 0