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Bone Research

Chengjie Lian, Xudong Wang, Xianjian Qiu, Zizhao Wu, Bo Gao, Lei Liu, Guoyan Liang, Hang Zhou, Xiaoming Yang, Yan Peng, Anjing Liang, Caixia Xu, Dongsheng Huang, Peiqiang Su
Hypertrophic differentiation is not only the terminal process of endochondral ossification in the growth plate but is also an important pathological change in osteoarthritic cartilage. Collagen type II (COL2A1) was previously considered to be only a structural component of the cartilage matrix, but recently, it has been revealed to be an extracellular signaling molecule that can significantly suppress chondrocyte hypertrophy. However, the mechanisms by which COL2A1 regulates hypertrophic differentiation remain unclear...
2019: Bone Research
Delphine B Maurel, Tsutomu Matsumoto, Julian A Vallejo, Mark L Johnson, Sarah L Dallas, Yukiko Kitase, Marco Brotto, Michael J Wacker, Marie A Harris, Stephen E Harris, Lynda F Bonewald
Transgenic mice are widely used to delete or overexpress genes in a cell specific manner to advance knowledge of bone biology, function and disease. While numerous Cre models exist to target gene recombination in osteoblasts and osteoclasts, few target osteocytes specifically, particularly mature osteocytes. Our goal was to create a spatial and temporal conditional Cre model using tamoxifen to induce Cre activity in mature osteocytes using a Bac construct containing the 5' and 3' regions of the Sost gene (Sost ERT2 Cre)...
2019: Bone Research
Christophe Merceron, Kavitha Ranganathan, Elizabeth Wang, Zachary Tata, Shreya Makkapati, Mohd Parvez Khan, Laura Mangiavini, Angela Qing Yao, Laura Castellini, Benjamin Levi, Amato J Giaccia, Ernestina Schipani
Osteoblasts, which are the bone-forming cells, operate in a hypoxic environment. The transcription factors hypoxia-inducible factor-1α (HIF1) and HIF2 are key mediators of the cellular response to hypoxia. Both are expressed in osteoblasts. HIF1 is known to be a positive regulator of bone formation. Conversely, the role of HIF2 in the control osteoblast biology is still poorly understood. In this study, we used mouse genetics to demonstrate that HIF2 is an inhibitor of osteoblastogenesis and bone mass accrual...
2019: Bone Research
Chuangxin Lin, Liangliang Liu, Chun Zeng, Zhong-Kai Cui, Yuhui Chen, Pinling Lai, Hong Wang, Yan Shao, Haiyan Zhang, Rongkai Zhang, Chang Zhao, Hang Fang, Daozhang Cai, Xiaochun Bai
Increasing evidences show that aberrant subchondral bone remodeling plays an important role in the development of osteoarthritis (OA). However, how subchondral bone formation is activated and the mechanism by which increased subchondral bone turnover promotes cartilage degeneration during OA remains unclear. Here, we show that the mechanistic target of rapamycin complex 1 (mTORC1) pathway is activated in subchondral bone preosteoblasts (Osterix+) from OA patients and mice. Constitutive activation of mTORC1 in preosteoblasts by deletion of the mTORC1 upstream inhibitor, tuberous sclerosis 1, induced aberrant subchondral bone formation, and sclerosis with little-to-no effects on articular cartilage integrity, but accelerated post-traumatic OA development in mice...
2019: Bone Research
Yong Xie, Shaohua Zhan, Wei Ge, Peifu Tang
No abstract text is available yet for this article.
2019: Bone Research
Minhao Gao, Weiyang Gao, J M Papadimitriou, Changqing Zhang, Junjie Gao, Minghao Zheng
[This corrects the article DOI: 10.1038/s41413-018-0039-2.].
2019: Bone Research
Robert Brommage, Jeff Liu, Peter Vogel, Faika Mseeh, Andrea Y Thompson, David G Potter, Melanie K Shadoan, Gwenn M Hansen, Sabrina Jeter-Jones, Jie Cui, Dawn Bright, Jennifer P Bardenhagen, Deon D Doree, Sofia Movérare-Skrtic, Karin H Nilsson, Petra Henning, Ulf H Lerner, Claes Ohlsson, Arthur T Sands, James E Tarver, David R Powell, Brian Zambrowicz, Qingyun Liu
The disability, mortality and costs caused by non-vertebral osteoporotic fractures are enormous. Existing osteoporosis therapies are highly effective at reducing vertebral but not non-vertebral fractures. Cortical bone is a major determinant of non-vertebral bone strength. To identify novel osteoporosis drug targets, we phenotyped cortical bone of 3 366 viable mouse strains with global knockouts of druggable genes. Cortical bone thickness was substantially elevated in Notum -/- mice. NOTUM is a secreted WNT lipase and we observed high NOTUM expression in cortical bone and osteoblasts but not osteoclasts...
2019: Bone Research
Yuta Nakai, Kazuo Okamoto, Asuka Terashima, Shogo Ehata, Jun Nishida, Takeshi Imamura, Takashi Ono, Hiroshi Takayanagi
Bone is one of the preferred sites for the metastasis of malignant tumours, such as breast cancer, lung cancer and malignant melanoma. Tumour cells colonizing bone have the capacity to induce the expression of receptor activator of nuclear factor-κB ligand (RANKL), which promotes osteoclast differentiation and activation. Tumour-induced osteoclastic bone resorption leads to a vicious cycle between tumours and bone cells that fuels osteolytic tumour growth, causing bone pain and hypercalcaemia. Furthermore, RANKL contributes to bone metastasis by acting as a chemoattractant to bone for tumour cells that express its receptor, RANK...
2019: Bone Research
Yuxin Zhang, Wenjuan Ma, Yuxi Zhan, Chenchen Mao, Xiaoru Shao, Xueping Xie, Xiawei Wei, Yunfeng Lin
With the incidence of different bone diseases increasing, effective therapies are needed that coordinate a combination of various technologies and biological materials. Bone tissue engineering has also been considered as a promising strategy to repair various bone defects. Therefore, different biological materials that can promote stem cell proliferation, migration, and osteoblastic differentiation to accelerate bone tissue regeneration and repair have also become the focus of research in multiple fields. Stem cell therapy, biomaterial scaffolds, and biological growth factors have shown potential for bone tissue engineering; however, off-target effects and cytotoxicity have limited their clinical use...
2018: Bone Research
Minhao Gao, Weiyang Gao, J M Papadimitriou, Changqing Zhang, Junjie Gao, Minghao Zheng
Exosomes are a heterogeneous group of cell-derived membranous structures, which mediate crosstalk interaction between cells. Recent studies have revealed a close relationship between exosomes and bone homeostasis. It is suggested that bone cells can spontaneously secret exosomes containing proteins, lipids and nucleic acids, which then to regulate osteoclastogenesis and osteogenesis. However, the network of regulatory activities of exosomes in bone homeostasis as well as their therapeutic potential in bone injury remain largely unknown...
2018: Bone Research
Xu Cao
No abstract text is available yet for this article.
2018: Bone Research
Xiao Chen, Xin Zhi, Jun Wang, Jiacan Su
RANKL signaling is essential for osteoclastogenesis. Its role in osteoblastic differentiation and bone formation is unknown. Here we demonstrate that RANK is expressed at an early stage of bone marrow mesenchymal stem cells (BMSCs) during osteogenic differentiation in both mice and human and decreased rapidly. RANKL signaling inhibits osteogenesis by promoting β-catenin degradation and inhibiting its synthesis. In contrast, RANKL signaling has no significant effects on adipogenesis of BMSCs. Interestingly, conditional knockout of rank in BMSCs with Prx1 -Cre mice leads to a higher bone mass and increased trabecular bone formation independent of osteoclasts...
2018: Bone Research
Ruoshi Xu, Sanjoy Kumar Khan, Taifeng Zhou, Bo Gao, Yaxing Zhou, Xuedong Zhou, Yingzi Yang
How osteoblast cells are induced is a central question for understanding skeletal formation. Abnormal osteoblast differentiation leads to a broad range of devastating craniofacial diseases. Here we have investigated intramembranous ossification during cranial bone development in mouse models of skeletal genetic diseases that exhibit craniofacial bone defects. The GNAS gene encodes Gαs that transduces GPCR signaling. GNAS activation or loss-of-function mutations in humans cause fibrous dysplasia (FD) or progressive osseous heteroplasia (POH) that shows craniofacial hyperostosis or craniosynostosis, respectively...
2018: Bone Research
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
The adaptor protein NUMB is involved in asymmetric division and cell fate determination and recognized as an antagonist of Notch. Previous 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)...
2018: Bone Research
Ke Zhang, Suping Wang, Chenchen Zhou, Lei Cheng, Xianling Gao, Xianju Xie, Jirun Sun, Haohao Wang, Michael D Weir, Mark A Reynolds, Ning Zhang, Yuxing Bai, Hockin H K Xu
Hard tissue repair and regeneration cost hundreds of billions of dollars annually worldwide, and the need has substantially increased as the population has aged. Hard tissues include bone and tooth structures that contain calcium phosphate minerals. Smart biomaterial-based tissue engineering and regenerative medicine methods have the exciting potential to meet this urgent need. Smart biomaterials and constructs refer to biomaterials and constructs that possess instructive/inductive or triggering/stimulating effects on cells and tissues by engineering the material's responsiveness to internal or external stimuli or have intelligently tailored properties and functions that can promote tissue repair and regeneration...
2018: Bone Research
Yuxing Guo, Yuan Yuan, Ling Wu, Thach-Vu Ho, Junjun Jing, Hideki Sugii, Jingyuan Li, Xia Han, Jifan Feng, Chuanbin Guo, Yang Chai
Calvarial bones are connected by fibrous sutures. These sutures provide a niche environment that includes mesenchymal stem cells (MSCs), osteoblasts, and osteoclasts, which help maintain calvarial bone homeostasis and repair. Abnormal function of osteogenic cells or diminished MSCs within the cranial suture can lead to skull defects, such as craniosynostosis. Despite the important function of each of these cell types within the cranial suture, we have limited knowledge about the role that crosstalk between them may play in regulating calvarial bone homeostasis and injury repair...
2018: Bone Research
J Edward Puzas
No abstract text is available yet for this article.
2018: Bone Research
Ye Li, Xinxin Wang, Jiali Ren, Xiaoshan Wu, Guoqing Li, Zhipeng Fan, Chunmei Zhang, Ang Li, Songlin Wang
Signal transduction between different organs is crucial in the normal development of the human body. As an important medium for signal communication, exosomes can transfer important information, such as microRNAs (miRNAs), from donors to receptors. MiRNAs are known to fine-tune a variety of biological processes, including maxillofacial development; however, the underlying mechanism remains largely unknown. In the present study, transient apoptosis was found to be due to the expression of a miniature swine maxillofacial-specific miRNA, ssc-mir-133b...
2018: Bone Research
Wenjia Liu, Liqiang Zhang, Kun Xuan, Chenghu Hu, Shiyu Liu, Li Liao, Bei Li, Fang Jin, Songtao Shi, Yan Jin
Mutations in the liver/bone/kidney alkaline phosphatase ( Alpl ) gene cause hypophosphatasia (HPP) and early-onset bone dysplasia, suggesting that this gene is a key factor in human bone development. However, how and where Alpl acts in bone ageing is largely unknown. Here, we determined that ablation of Alpl induces prototypical premature bone ageing characteristics, including bone mass loss and marrow fat gain coupled with elevated expression of p16INK4A (p16) and p53 due to senescence and impaired differentiation in mesenchymal stem cells (MSCs)...
2018: Bone Research
Liwei Zheng, Caixia Pi, Jun Zhang, Yi Fan, Chen Cui, Yang Zhou, Jianxun Sun, Quan Yuan, Xin Xu, Ling Ye, Xu Cao, Xuedong Zhou
There is currently no effective medical treatment for temporomandibular joint osteoarthritis (TMJ-OA) due to a limited understanding of its pathogenesis. This study was undertaken to investigate the key role of transforming growth factor-β (TGF-β) signalling in the cartilage and subchondral bone of the TMJ using a temporomandibular joint disorder (TMD) rat model, an ageing mouse model and a Camurati-Engelmann disease (CED) mouse model. In the three animal models, the subchondral bone phenotypes in the mandibular condyles were evaluated by µCT, and changes in TMJ condyles were examined by TRAP staining and immunohistochemical analysis of Osterix and p-Smad2/3...
2018: Bone Research
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