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Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA
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Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA
Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA
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%). Tibial cortical parameters were also significantly affected in the KO mice showing decrease in cortical BMC (10%), and TMD (3%). Bone histomorphometry revealed a reduced trabecular bone formation in Mkp1 KO compared with WT female mice (KO 4
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extracellular acidification ( Palokangas et al . 1997 , Mellis et al . 2011 ). Like bone formation, this is under tight control by a variety of autocrine, paracrine, and endocrine factors and is thought to be primarily regulated by the terminally
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osteoblast functions. In this study, we establish that miR-487b-3p negatively controls osteogenesis by obstructing Notch-regulated ankyrin-repeat protein (Nrarp) which blocks Notch signaling and promotes bone formation. Materials and methods
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Department of Genetics and Molecular Biology, University of Campinas, São Paulo, Brazil
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Department of Medicine, The University of Melbourne, St. Vincent’s Hospital, Melbourne, Australia
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Department of Medicine, The University of Melbourne, St. Vincent’s Hospital, Melbourne, Australia
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consolidation and did not rescue the phenotype of Dmp1cre.Socs3 fl/fl mice. Leptin receptor deficiency delayed bone consolidation only in female mice. One explanation for this may arise from the sex-dependent levels of bone formation and resorption in male
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Department of Women’s and Children’s Health, Karolinska Institutet and Pediatric Endocrinology Unit, Karolinska University Hospital, Stockholm, Sweden
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rates of bone growth, their skeleton is particularly vulnerable to the adverse effects of GCs on bone formation. GC-induced growth retardation was first described 60 years ago after an equivalent cortisone dose of only 1.5 mg/kg/day ( Blodgett et al
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changes in bone were a result of impaired bone formation, whilst resorption was normal. The reduced formation may be a consequence of altered signalling pathways such as the GH/IGF1 axis that is known to be anabolic to the skeleton. These changes resemble
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
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Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
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Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
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Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
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Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
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Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
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Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
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Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
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Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
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Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
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compartment. The bone sparing effects of estrogen in rodents are believed not only to be mediated through inhibition of bone resorption, but also through stimulation of bone formation ( Chow et al. 1992 ). However, some studies indicate that the effects of
Center for Healthy Aging Research, Oregon State University, Corvallis, Oregon, USA
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Center for Healthy Aging Research, Oregon State University, Corvallis, Oregon, USA
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surface. Modeling refers to changes in bone architecture where bone is added to a preexisting bone surface without a requirement for prior bone resorption or by which bone is resorbed from a bone surface without initiating subsequent bone formation
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chondrocytes synthesise type X collagen, which induces cartilage mineralisation, thus generating a template for osteoblastic bone formation. Epiphyseal growth plates form at either end of the anlage and consist of organised columns of proliferating
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). This is the likely basis of ACTH action in preventing glucocorticoid-induced osteonecrosis, as assessed in a rabbit model ( Zaidi et al . 2010 ). Figure 1 Endocrine control of bone remodeling. Bone formation is regulated by signals from