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that cause excessive or impaired bone loss impact skeletal integrity as well as the immoderate, disorganised or reduced bone formation ( Del Fattore et al. 2012 ). Osteoblasts, the bone-making cells, derive from neural ectoderm to form craniofacial
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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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and total bone mass ( Hamrick et al . 2004 , Ealey et al . 2006 , Gat-Yablonski & Phillip 2008 , Williams et al . 2011 ). At the cellular level, these abnormalities are associated with impaired endochondral ossification, lower bone formation due
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Departments of Pharmacology, Orthodontics, Transcriptome Research Group, Department of Developmental Biology of Hard Tissue, Department of Molecular Pharmacology, School of Dental Medicine, Tsurumi University, 2‐1‐3 Tsurumi, Tsurumi‐ku, Yokohama 230-8501, Japan
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Departments of Pharmacology, Orthodontics, Transcriptome Research Group, Department of Developmental Biology of Hard Tissue, Department of Molecular Pharmacology, School of Dental Medicine, Tsurumi University, 2‐1‐3 Tsurumi, Tsurumi‐ku, Yokohama 230-8501, Japan
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osteoblasts may be exerted through activation of ERKs ( Bellido & Plotkin 2011 ). Local application of N-BPs has been shown to promote bone formation around N-BP-coated implants in vivo ( Tanzer et al . 2005 , Gao et al . 2009 ). Previously, we reported
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Department of Geriatric Medicine, Department of Developmental and Cell Biology, Division of Radiology, Department of Anti-Aging Medicine, Division of Gene Regulation and Signal Transduction, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
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Department of Geriatric Medicine, Department of Developmental and Cell Biology, Division of Radiology, Department of Anti-Aging Medicine, Division of Gene Regulation and Signal Transduction, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
Department of Geriatric Medicine, Department of Developmental and Cell Biology, Division of Radiology, Department of Anti-Aging Medicine, Division of Gene Regulation and Signal Transduction, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
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understand the roles of SXR/PXR in the bone tissue more precisely. Our results demonstrated that loss of SXR/PXR enhanced bone resorption and reduced bone formation in the trabecular bones and decreased thickness in the cortical bones. Moreover, these mice
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physiological bone formation and pathological vascular calcification, and provides an overview of how these can be regulated by local and systemic factors. Bone formation Bone is a composite tissue comprised of both organic and mineral components
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The Institute for Pharmacology and Toxicology, University of Bonn, Bonn, Germany
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bone are cGMP independent ( van’t Hof & Ralston 2001 , Wimalawansa 2007 , Kalyanaraman et al. 2018 a ). To examine the role of PKG2 in post-natal bone acquisition, independently of its function in endochondral bone formation, we established
St.Vincent's Institute of Medical Research, Department of Medicine at St. Vincent's Hospital Melbourne, Department of Cancer Research and Molecular Medicine, 9 Princes St, Fitzroy, Victoria 3065, Australia
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St.Vincent's Institute of Medical Research, Department of Medicine at St. Vincent's Hospital Melbourne, Department of Cancer Research and Molecular Medicine, 9 Princes St, Fitzroy, Victoria 3065, Australia
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St.Vincent's Institute of Medical Research, Department of Medicine at St. Vincent's Hospital Melbourne, Department of Cancer Research and Molecular Medicine, 9 Princes St, Fitzroy, Victoria 3065, Australia
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for osteoporosis capable of inducing bone formation (reviewed in Hodsman et al . (2005) and Khosla et al . (2008) ). However, the mechanisms by which intermittent PTH increases bone mass remain unclear, and identifying downstream targets of this
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Prostaglandin E(2) (PGE(2)) has been shown to exert a bone anabolic effect in young and adult rats. In this study we tested whether it possesses a similar effect on bone formation and bone mass in aging rats. Fifteen-month-old rats were injected daily with either PGE(2) at 5 mg/kg or vehicle for 14 days. PGE(2) treatment stimulated the rate of cancellous bone formation (a approximately 5.5-fold increase in bone formation rate), measured by the incorporation of calcein into bone-forming surfaces at the tibial proximal metaphysis. This effect resulted in increased cancellous bone area (+54%) at the same site. Since PGE(2) treatment resulted in a much higher proportion of bone surface undergoing bone formation and thus lined with osteoblasts, we tested the hypothesis that PGE(2) stimulates osteoblast differentiation from bone marrow precursor cells both in vivo and in vitro. We found that ex vivo cultures of bone marrow stromal cells from rats injected for 2 weeks with PGE(2) at 5 mg/kg per day yielded more ( approximately 4-fold) mineralized nodules and exhibited a greater (by 30-40%) alkaline phosphatase activity compared with cultures from vehicle-injected rats, attesting to a stimulation of osteoblastic differentiation by PGE(2). We also compared the osteogenic capacity of bone marrow from aging (15-month-old) versus young (5-week-old) rats and its regulation by PGE(2) in vitro. Bone marrow stromal cell cultures from aging rats exhibited a greatly diminished osteogenic capacity, reflected in reduced nodule formation ( approximately 6% of young animals) and lower alkaline phosphatase activity ( approximately 60% of young animals). However, these parameters could be stimulated in both groups of animals by incubation with 10-100 nM PGE(2). The magnitude of this stimulation was greater in cultures from aging rats (+550% vs +70% in nodule formation of aging compared with young rats). In conclusion, we demonstrate here that PGE(2) exerts a bone anabolic effect in aging rats, similar to the effect we and others have reported in young, growing rats. The PGE(2)-stimulated bone formation, which augments bone mass, most likely results from recruitment of osteoblasts from their bone marrow stromal precursors.
Center for Health Disparities and Molecular Medicine, School of Medicine, Loma Linda University, Loma Linda, California, USA
Division of Biochemistry, Department of Basic Sciences, School of Medicine, Loma Linda University, Loma Linda, California, USA
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Center for Health Disparities and Molecular Medicine, School of Medicine, Loma Linda University, Loma Linda, California, USA
Division of Biochemistry, Department of Basic Sciences, School of Medicine, Loma Linda University, Loma Linda, California, USA
Department of Medicine, School of Medicine, Loma Linda University, Loma Linda, California, USA
Department of Orthopedics, School of Medicine, Loma Linda University, Loma Linda, California, USA
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Introduction Osteoporosis, a debilitating condition in which an increase in bone resorption is not adequately compensated by a corresponding increase in bone formation, leading to net loss of bone mass and microarchitectural deterioration
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, an elevated level of insulin in PCOS women leads to insulin resistance resulting in the deterioration of BMD. Effect of insulin resistance on bone in PCOS women Insulin signaling attenuates bone formation by decreasing the expression of
