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Bibliographies thématiques / Bone cells Metabolism / Articles de revues

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Articles de revues sur le sujet « Bone cells Metabolism »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 28 janvier 2023

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1

INOUE, HIROMASA. "Cells phagocytizing bone. Bone metabolism and osteoclast." Kagaku To Seibutsu 23, no. 2 (1985): 99–102. http://dx.doi.org/10.1271/kagakutoseibutsu1962.23.99.

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Shymanskyy, I. O., O. O. Lisakovska, A. O. Mazanova, D. O. Labudzynskyi, A. V. Khomenko, and M. M. Veliky. "Prednisolone and vitamin D(3) modulate oxidative metabolism and cell death pathways in blood and bone marrow mononuclear cells." Ukrainian Biochemical Journal 88, no. 5 (October 31, 2016): 38–47. http://dx.doi.org/10.15407/ubj88.05.038.

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Locci, P., E. Becchetti, G. Venti, C. Lilli, L. Marinucci, E. Donti, G. Paludetti, and M. Maurizi. "Glycosaminoglycan metabolism in otosclerotic bone cells." Biology of the Cell 86, no. 1 (1996): 73–78. http://dx.doi.org/10.1111/j.1768-322x.1996.tb00958.x.

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Barry, Patrick. "Skeletal discovery: Bone cells affect metabolism." Science News 172, no. 6 (September 30, 2009): 83. http://dx.doi.org/10.1002/scin.2007.5591720602.

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Motyl, Katherine J., Anyonya R. Guntur, Adriana Lelis Carvalho, and Clifford J. Rosen. "Energy Metabolism of Bone." Toxicologic Pathology 45, no. 7 (October 2017): 887–93. http://dx.doi.org/10.1177/0192623317737065.

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Biological processes utilize energy and therefore must be prioritized based on fuel availability. Bone is no exception to this, and the benefit of remodeling when necessary outweighs the energy costs. Bone remodeling is important for maintaining blood calcium homeostasis, repairing micro cracks and fractures, and modifying bone structure so that it is better suited to withstand loading demands. Osteoclasts, osteoblasts, and osteocytes are the primary cells responsible for bone remodeling, although bone marrow adipocytes and other cells may also play an indirect role. There is a renewed interes

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Kumegawa, Masayoshi. "Role of Bone Cells in Bone Metabolism : Osteoclasts and Osteocytes." Journal of the Kyushu Dental Society 48, no. 5 (1994): 640–43. http://dx.doi.org/10.2504/kds.48.640.

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Ruzicska, Éva, and Gyula Poór. "Diabetes and bone metabolism." Orvosi Hetilap 152, no. 29 (July 2011): 1156–60. http://dx.doi.org/10.1556/oh.2011.29147.

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In the past decade several novel findings point to the critical role of the skeleton in several homeostatic processes, including energy balance. The connection begins in the bone marrow with lineage allocation of mesenchymal stem cells to adipocytes or osteoblasts. Osteoblasts and adipocytes produce factors affecting insulin homeostasis. The hormonally active adipose tissue can regulate bone metabolism. In this review authors discuss targets taking critical part in the bone-fat network: leptin, osteocalcin, PPAR γ2 and the Wnt/beta catenin pathway. Leptin regulates energy metabolism through co

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Anderson, Paul H., Gerald J. Atkins, Andrew G. Turner, Masakazu Kogawa, David M. Findlay, and Howard A. Morris. "Vitamin D metabolism within bone cells: Effects on bone structure and strength." Molecular and Cellular Endocrinology 347, no. 1-2 (December 2011): 42–47. http://dx.doi.org/10.1016/j.mce.2011.05.024.

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Kim, Haemin, Brian Oh, and Kyung-Hyun Park-Min. "Regulation of Osteoclast Differentiation and Activity by Lipid Metabolism." Cells 10, no. 1 (January 7, 2021): 89. http://dx.doi.org/10.3390/cells10010089.

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Bone is a dynamic tissue and is constantly being remodeled by bone cells. Metabolic reprogramming plays a critical role in the activation of these bone cells and skeletal metabolism, which fulfills the energy demand for bone remodeling. Among various metabolic pathways, the importance of lipid metabolism in bone cells has long been appreciated. More recent studies also establish the link between bone loss and lipid-altering conditions—such as atherosclerotic vascular disease, hyperlipidemia, and obesity—and uncover the detrimental effect of fat accumulation on skeletal homeostasis and increase

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Kim, Haemin, Brian Oh, and Kyung-Hyun Park-Min. "Regulation of Osteoclast Differentiation and Activity by Lipid Metabolism." Cells 10, no. 1 (January 7, 2021): 89. http://dx.doi.org/10.3390/cells10010089.

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Bone is a dynamic tissue and is constantly being remodeled by bone cells. Metabolic reprogramming plays a critical role in the activation of these bone cells and skeletal metabolism, which fulfills the energy demand for bone remodeling. Among various metabolic pathways, the importance of lipid metabolism in bone cells has long been appreciated. More recent studies also establish the link between bone loss and lipid-altering conditions—such as atherosclerotic vascular disease, hyperlipidemia, and obesity—and uncover the detrimental effect of fat accumulation on skeletal homeostasis and increase

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Wang, Qingxuan, Mengmeng Duan, Jingfeng Liao, Jing Xie, and Chenchen Zhou. "Are Osteoclasts Mechanosensitive Cells?" Journal of Biomedical Nanotechnology 17, no. 10 (October 1, 2021): 1917–38. http://dx.doi.org/10.1166/jbn.2021.3171.

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Skeleton metabolism is a process in which osteoclasts constantly remove old bone and osteoblasts form new osteoid and induce mineralization; disruption of this balance may cause diseases. Osteoclasts play a key role in bone metabolism, as osteoclastogenesis marks the beginning of each bone remodeling cycle. As the only cell capable of bone resorption, osteoclasts are derived from the monocyte/macrophage hematopoietic precursors that terminally adhere to mineralized extracellular matrix, and they subsequently break down the extracellular compartment. Bone is generally considered the load-burden

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Aubin, Jane E. "Bone blood stem cells." Bone 43 (October 2008): S15—S16. http://dx.doi.org/10.1016/j.bone.2008.07.018.

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Zeng, Zhipeng, Xuchang Zhou, Yan Wang, Hong Cao, Jianmin Guo, Ping Wang, Yajing Yang, and Yan Wang. "Mitophagy—A New Target of Bone Disease." Biomolecules 12, no. 10 (October 4, 2022): 1420. http://dx.doi.org/10.3390/biom12101420.

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Bone diseases are usually caused by abnormal metabolism and death of cells in bones, including osteoblasts, osteoclasts, osteocytes, chondrocytes, and bone marrow mesenchymal stem cells. Mitochondrial dysfunction, as an important cause of abnormal cell metabolism, is widely involved in the occurrence and progression of multiple bone diseases, including osteoarthritis, intervertebral disc degeneration, osteoporosis, and osteosarcoma. As selective mitochondrial autophagy for damaged or dysfunctional mitochondria, mitophagy is closely related to mitochondrial quality control and homeostasis. Accu

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Mankani, Mahesh H., and Pamela Gehron Robey. "Transplantation of Bone-Forming Cells." Endocrinologist 8, no. 6 (November 1998): 459–68. http://dx.doi.org/10.1097/00019616-199811000-00009.

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Qaw, Fuad S., Hugh L. J. Makin, and Glenville Jones. "Metabolism of 25-hydroxydihydrotachysterol3 in bone cells in vitro." Steroids 57, no. 5 (May 1992): 236–43. http://dx.doi.org/10.1016/0039-128x(92)90108-l.

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Westacott, Carole I., Ginette R. Webb, Mark G. Warnock, Jane V. Sims, and Christopher J. Elson. "Alteration of cartilage metabolism by cells from osteoarthritic bone." Arthritis & Rheumatism 40, no. 7 (July 1997): 1282–91. http://dx.doi.org/10.1002/1529-0131(199707)40:7<1282::aid-art13>3.0.co;2-e.

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Compston, JE. "Bone marrow and bone: a functional unit." Journal of Endocrinology 173, no. 3 (June 1, 2002): 387–94. http://dx.doi.org/10.1677/joe.0.1730387.

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Bone and bone marrow, although often regarded as separate systems, function as a single unit. Cells in the bone marrow are the precursors of bone remodelling cells and exert an important regulatory role both on their own development and the remodelling process, acting as mediators for the effects of systemic and local factors. Other cells, such as immune cells and megakaryocytes, also contribute to the regulation of bone cell development and activity. Many diseases that affect the bone marrow have profound effects on bone, involving interactions between abnormal and normal marrow cells and tho

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Zhou, Xuchang, Hong Cao, Jianming Guo, Yu Yuan, and Guoxin Ni. "Effects of BMSC-Derived EVs on Bone Metabolism." Pharmaceutics 14, no. 5 (May 8, 2022): 1012. http://dx.doi.org/10.3390/pharmaceutics14051012.

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Extracellular vesicles (EVs) are small membrane vesicles that can be secreted by most cells. EVs can be released into the extracellular environment through exocytosis, transporting endogenous cargo (proteins, lipids, RNAs, etc.) to target cells and thereby triggering the release of these biomolecules and participating in various physiological and pathological processes. Among them, EVs derived from bone marrow mesenchymal stem cells (BMSC-EVs) have similar therapeutic effects to BMSCs, including repairing damaged tissues, inhibiting macrophage polarization and promoting angiogenesis. In additi

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Phulpin, Bérengère, Gilles Dolivet, Pierre-Yves Marie, Sylvain Poussier, Sandrine Huger, Pierre Bravetti, Pierre Graff, Jean-Louis Merlin, and Nguyen Tran. "Feasibility of Treating Irradiated Bone with Intramedullary Delivered Autologous Mesenchymal Stem Cells." Journal of Biomedicine and Biotechnology 2011 (2011): 1–9. http://dx.doi.org/10.1155/2011/560257.

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Background. We aimed to explore (i) the short-term retention of intramedullary implanted mesenchymal stem cells BMSCs and (ii) their impact on the bone blood flow and metabolism in a rat model of hindlimb irradiation.Methods. Three months after 30 Gy irradiation, fourteen animals were referred into 2 groups: a sham-operated group (n=6) and a treated group (n=8) in which111In-labelled BMSCs (2×106cells) were injected in irradiated tibias. Bone blood flow and metabolism were assessed by serialT99mc-HDP scintigraphy and 1-wk cell retention by recordings ofT99mc/111In activities.Results. The amoun

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Zhou, Tao, Yuqing Yang, Qianming Chen, and Liang Xie. "Glutamine Metabolism Is Essential for Stemness of Bone Marrow Mesenchymal Stem Cells and Bone Homeostasis." Stem Cells International 2019 (September 12, 2019): 1–13. http://dx.doi.org/10.1155/2019/8928934.

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Skeleton has emerged as an endocrine organ which is both capable of regulating energy metabolism and being a target for it. Glutamine is the most bountiful and flexible amino acid in the body which provides adenosine 5′-triphosphate (ATP) demands for cells. Emerging evidences support that glutamine which acts as the second metabolic regulator after glucose exerts crucial roles in bone homeostasis at cellular level, including the lineage allocation and proliferation of bone mesenchymal stem cells (BMSCs), the matrix mineralization of osteoblasts, and the biosynthesis in chondrocytes. The integr

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Lyu, Zhong-Shi, Wei-Li Yao, Qi Wen, Hong-Yan Zhao, Fei-Fei Tang, Yu Wang, Lan-Ping Xu, et al. "Glycolysis Restoration Attenuates Damaged Bone Marrow Endothelial Cells." Blood 134, Supplement_1 (November 13, 2019): 2491. http://dx.doi.org/10.1182/blood-2019-122794.

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Background: Bone marrow(BM) endothelial cells(ECs), a key component of BM microenvironment, is essential for the physiology and regeneration of hematopoietic stem cells (HSCs). The damage of ECs is recognized by us and other researchers as a mainstay in the pathophysiology of a serious of life-threatening complications after chemoradiotherapy and myeloablative hematopoietic cell transplantation(HSCT), including poor graft function (PGF) (2013BBMT, 2015BMT, 2016Blood, 2019Blood Advances). Despite numerous researches focused on the BM ECs contributing to HSC regeneration following myelotoxicity,

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Gromova, О. А., А. М. Lila, I. Yu Torshin, and I. А. Reier. "Application of chondroprotective agents to inhibit osteodestructive processes in the subchondral bone in patients with osteoarthritis." FARMAKOEKONOMIKA. Modern Pharmacoeconomics and Pharmacoepidemiology 15, no. 1 (March 15, 2022): 107–18. http://dx.doi.org/10.17749/2070-4909/farmakoekonomika.2022.126.

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Background. Osteoarthritis (OA) is associated with an activation of local inflammation and involves subchondral tissue of the joint.Objective: to conduct a systemic analysis of the publications on the association between OA and metabolic disorders in bones.Material and methods. The authors analyzed 3,926 publications on the studies of OA and metabolic disorders in bones tissue by the method of a topologic theory of recognition selected by the request “osteoarthritis AND (bone resorption OR osteopenia OR osteoporosis)” in the database of biomedical publications PubMed/MEDLINE. The control sampl

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Gallagher, J. A., J. P. Dillon, and C. E. Sheard. "Rhinoceros bone cells in culture." Bone 7, no. 4 (1986): 313. http://dx.doi.org/10.1016/8756-3282(86)90247-4.

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Adams⁎, G. B. "Hematopoietic stem cells and bone☆." Bone 47 (June 2010): S22. http://dx.doi.org/10.1016/j.bone.2010.04.025.

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Yankova, I., A. Shinkov, and R. Kovatcheva. "Changes in Bone Metabolism and Structure in Primary Hyperparathyroidism." Acta Medica Bulgarica 47, no. 4 (November 1, 2020): 75–80. http://dx.doi.org/10.2478/amb-2020-0050.

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AbstractParathyroid hormone (PTH) is a key regulator of bone turnover. Depending on the duration of action, the hormone causes catabolic and anabolic effects by binding with specific receptors (PTHR1) in the bone. Various cells expressing PTHR1 on their surface are involved in the process – osteoblasts, osteocytes, bone marrow stromal cells, T-lymphocytes and macrophages. In physiological conditions PTH balances the bone metabolism. Intermittent pharmacological doses of PTH lead to the prevalence of bone formation and are used in the treatment of osteoporosis. Persistently elevated levels of P

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Riddle, Ryan C., and Thomas L. Clemens. "Bone Cell Bioenergetics and Skeletal Energy Homeostasis." Physiological Reviews 97, no. 2 (April 2017): 667–98. http://dx.doi.org/10.1152/physrev.00022.2016.

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The rising incidence of metabolic diseases worldwide has prompted renewed interest in the study of intermediary metabolism and cellular bioenergetics. The application of modern biochemical methods for quantitating fuel substrate metabolism with advanced mouse genetic approaches has greatly increased understanding of the mechanisms that integrate energy metabolism in the whole organism. Examination of the intermediary metabolism of skeletal cells has been sparked by a series of unanticipated observations in genetically modified mice that suggest the existence of novel endocrine pathways through

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Yin, Wenzhen, Ziru Li, and Weizhen Zhang. "Modulation of Bone and Marrow Niche by Cholesterol." Nutrients 11, no. 6 (June 21, 2019): 1394. http://dx.doi.org/10.3390/nu11061394.

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Bone is a complex tissue composing of mineralized bone, bone cells, hematopoietic cells, marrow adipocytes, and supportive stromal cells. The homeostasis of bone and marrow niche is dynamically regulated by nutrients. The positive correlation between cardiovascular disease and osteoporosis risk suggests a close relationship between hyperlipidemia and/or hypercholesterolemia and the bone metabolism. Cholesterol and its metabolites influence the bone homeostasis through modulating the differentiation and activation of osteoblasts and osteoclasts. The effects of cholesterol on hematopoietic stem

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Tencerova, Michaela, Meshail Okla, and Moustapha Kassem. "Insulin Signaling in Bone Marrow Adipocytes." Current Osteoporosis Reports 17, no. 6 (November 20, 2019): 446–54. http://dx.doi.org/10.1007/s11914-019-00552-8.

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Abstract Purpose of Review The goal of this review is to discuss the role of insulin signaling in bone marrow adipocyte formation, metabolic function, and its contribution to cellular senescence in relation to metabolic bone diseases. Recent Findings Insulin signaling is an evolutionally conserved signaling pathway that plays a critical role in the regulation of metabolism and longevity. Bone is an insulin-responsive organ that plays a role in whole body energy metabolism. Metabolic disturbances associated with obesity and type 2 diabetes increase a risk of fragility fractures along with incre

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Rothem, David E., Lilah Rothem, Michael Soudry, Aviva Dahan, and Rami Eliakim. "Nicotine modulates bone metabolism-associated gene expression in osteoblast cells." Journal of Bone and Mineral Metabolism 27, no. 5 (May 13, 2009): 555–61. http://dx.doi.org/10.1007/s00774-009-0075-5.

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Jones, D. B., and J. T. Ryaby. "Pulsed magnetic fields affect differentiation not metabolism in bone cells." Bone 7, no. 5 (January 1986): 396. http://dx.doi.org/10.1016/8756-3282(86)90292-9.

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Grayson, Warren L., Bruce A. Bunnell, Elizabeth Martin, Trivia Frazier, Ben P. Hung, and Jeffrey M. Gimble. "Stromal cells and stem cells in clinical bone regeneration." Nature Reviews Endocrinology 11, no. 3 (January 6, 2015): 140–50. http://dx.doi.org/10.1038/nrendo.2014.234.

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Prideaux, Matt, Tom O'Connell та Yukiko Kitase. "THE ROLE OF PPARδ-DRIVEN β-OXIDATION IN BONE HEALTH DURING AGING". Innovation in Aging 6, Supplement_1 (1 листопада 2022): 410. http://dx.doi.org/10.1093/geroni/igac059.1611.

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Abstract Musculoskeletal disorders are a significant complication of aging, leading to increased morbidity and mortality. However, current understanding of the mechanisms by which aging affects skeletal health is limited. Osteocytes are the most numerous and long-lived bone cells and play key roles in maintaining bone mass by responding to anabolic signals such as mechanical loading. Energy metabolism is dysregulated in many cells with aging, however regulation of energy metabolism in osteocytes and how this is affected during aging and by mechanical loading remains undefined. To investigate t

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Forsberg, Jonathan A., Thomas A. Davis, Eric A. Elster, and Jeffrey M. Gimble. "Burned to the Bone." Science Translational Medicine 6, no. 255 (September 24, 2014): 255fs37. http://dx.doi.org/10.1126/scitranslmed.3010168.

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Heterotopic ossification—a complication of severe burns, head or blast injuries, and orthopaedic trauma—can result from altered adenosine metabolism in mesenchymal stem cells in response to elevated extracellular ATP (Peterson et al., this issue).

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Chen, Qin, Krishna M. Sinha, Benoit de Crombrugghe, and Ralf Krahe. "Osteoblast-Specific Overexpression of Nucleolar Protein NO66/RIOX1 in Mouse Embryos Leads to Osteoporosis in Adult Mice." Journal of Osteoporosis 2023 (January 10, 2023): 1–10. http://dx.doi.org/10.1155/2023/8998556.

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In previous study, we showed that nucleolar protein 66 (NO66) is a chromatin modifier and negatively regulates Osterix activity as well as mesenchymal progenitor differentiation. Genetic ablation of the NO66 (RIOX1) gene in cells of the Prx1-expressing mesenchymal lineage leads to acceleration of osteochondrogenic differentiation and a larger skeleton in adult mice, whereas mesenchyme-specific overexpression of NO66 inhibits osteochondrogenesis resulting in dwarfism and osteopenia. However, the impact of NO66 overexpression in cells of the osteoblast lineage in vivo remains largely undefined.

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Shiraliyev, O. K., T. F. Mamedov, and Zh I. Gaghiyeva. "Hormones and osteoporosis." Problems of Endocrinology 40, no. 3 (December 15, 1994): 49–52. http://dx.doi.org/10.14341/probl12019.

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Osteoporosis and its complications - bone fractures - represent a significant medical and social problem. Due to osteoporosis, bone fractures occur annually in 1.3 million Americans and 40 thousand Canadians. In France, one in two, and in Australia, one in five women aged about 70 years, suffer from fractures caused by osteoporosis. The occurrence of osteoporosis in old women is due to a decrease in estrogen production. However, a decrease in bone mineral density occurs not only with age, but even more so with all conditions leading to a change in the balance of hormones of the hypothalamic-pi

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Srivastava, Rupesh K., Leena Sapra, and Pradyumna K. Mishra. "Osteometabolism: Metabolic Alterations in Bone Pathologies." Cells 11, no. 23 (December 6, 2022): 3943. http://dx.doi.org/10.3390/cells11233943.

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Renewing interest in the study of intermediate metabolism and cellular bioenergetics is brought on by the global increase in the prevalence of metabolic illnesses. Understanding of the mechanisms that integrate energy metabolism in the entire organism has significantly improved with the application of contemporary biochemical tools for quantifying the fuel substrate metabolism with cutting-edge mouse genetic procedures. Several unexpected findings in genetically altered mice have prompted research into the direction of intermediate metabolism of skeletal cells. These findings point to the poss

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Ishijima, Muneaki, Kunikazu Tsuji, Susan R. Rittling, Teruhito Yamashita, Hisashi Kurosawa, David T. Denhardt, Akira Nifuji, Yoichi Ezura, and Masaki Noda. "Osteopontin is required for mechanical stress-dependent signals to bone marrow cells." Journal of Endocrinology 193, no. 2 (May 2007): 235–43. http://dx.doi.org/10.1677/joe.1.06704.

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Mechanical stress to bone plays a crucial role in the maintenance of bone homeostasis. It causes the deformation of bone matrix and generates strain force, which could initiate the mechano-transduction pathway. The presence of osteopontin (OPN), which is one of the abundant proteins in bone matrix, is required for the effects of mechanical stress on bone, as we have reported that OPN-null (OPN−/−) mice showed resistance to unloading-induced bone loss. However, cellular mechanisms underlying the phenomenon have not been completely elucidated. To obtain further insight into the role of OPN in me

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Nyssen-Behets, C., D. Xhema, T. Schubert, M. Schubert, B. Lengelé, C. Delloye, and D. Dufrane. "Improvement of bone tissue allograft by mesenchymal stem cells: Bone marrow vs adipose stem cells." Bone 47 (June 2010): S128. http://dx.doi.org/10.1016/j.bone.2010.04.284.

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Hoebertz, A., A. Townsend-Nicholson, R. Glass, G. Burnstock, and T. R. Arnett. "Expression of P2 receptors in bone and cultured bone cells." Bone 27, no. 4 (October 2000): 503–10. http://dx.doi.org/10.1016/s8756-3282(00)00351-3.

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Cornish, Jillian, Usha Bava, Karen E. Callon, Jizhong Bai, Dorit Naot, and Ian R. Reid. "Bone-bound bisphosphonate inhibits growth of adjacent non-bone cells." Bone 49, no. 4 (October 2011): 710–16. http://dx.doi.org/10.1016/j.bone.2011.07.020.

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Fujita, Takuo. "Calcium, cells and bone." Journal of Bone and Mineral Metabolism 6, no. 1 (March 1988): 1–2. http://dx.doi.org/10.1007/bf02378732.

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Wang, Chunyu, Li Tian, Kun Zhang, Yaxi Chen, Xiang Chen, Ying Xie, Qian Zhao, and Xijie Yu. "Interleukin-6 gene knockout antagonizes high-fat-induced trabecular bone loss." Journal of Molecular Endocrinology 57, no. 3 (October 2016): 161–70. http://dx.doi.org/10.1530/jme-16-0076.

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The purpose of the study was to determine the roles of interleukin-6 (IL6) in fat and bone communication. Male wild-type (WT) mice and IL6 knockout (IL6−/−) mice were fed with either regular diet (RD) or high-fat diet (HFD) for 12 weeks. Bone mass and bone microstructure were evaluated by micro-computed tomography. Gene expression related to lipid and bone metabolisms was assayed with real-time quantitative polymerase chain reaction. Bone marrow cells from both genotypes were induced to differentiate into osteoblasts or osteoclasts, and treated with palmitic acid (PA). HFD increased the body w

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Singer, Frederick R., Barbara G. Mills, Helen E. Gruber, Jolene J. Windle, and G. David Roodman. "Ultrastructure of Bone Cells in Paget's Disease of Bone." Journal of Bone and Mineral Research 21, S2 (December 2006): P51—P54. http://dx.doi.org/10.1359/jbmr.06s209.

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Martin, Shailer B., William S. Reiche, Nicholas A. Fifelski, Alexander J. Schultz, Spencer J. Stanford, Alexander A. Martin, Danielle L. Nack, Bernhard Radlwimmer, Michael P. Boyer, and Elitsa A. Ananieva. "Leucine and branched-chain amino acid metabolism contribute to the growth of bone sarcomas by regulating AMPK and mTORC1 signaling." Biochemical Journal 477, no. 9 (May 5, 2020): 1579–99. http://dx.doi.org/10.1042/bcj20190754.

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Osteosarcoma and chondrosarcoma are sarcomas of the bone and the cartilage that are primarily treated by surgical intervention combined with high toxicity chemotherapy. In search of alternative metabolic approaches to address the challenges in treating bone sarcomas, we assessed the growth dependence of these cancers on leucine, one of the branched-chain amino acids (BCAAs), and BCAA metabolism. Tumor biopsies from bone sarcoma patients revealed differential expression of BCAA metabolic enzymes. The cytosolic branched-chain aminotransferase (BCATc) that is commonly overexpressed in cancer cell

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Allain, T. J., T. J. Chambers, A. M. Flanagan, and A. M. McGregor. "Tri-iodothyronine stimulates rat osteoclastic bone resorption by an indirect effect." Journal of Endocrinology 133, no. 3 (June 1992): 327–31. http://dx.doi.org/10.1677/joe.0.1330327.

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ABSTRACT Tri-iodothyronine (T3) increases bone resorption in vivo and in vitro. In order to understand further the mechanisms by which this occurs we studied the effects of T3 at concentrations in the range of 1 pmol/l–1 μmol/l on bone resorption by osteoclasts isolated from neonatal rat long bones. Osteoclasts were disaggregated and incubated either with or without UMR 106 cells or with mixed bone cells. We found that there was no effect of T3 on bone resorption by osteoclasts incubated alone or co-cultured with UMR 106 cells. However, in culture with mixed bone cells there was a significant

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Anastasilakis, Athanasios D., Marina Tsoli, Gregory Kaltsas, and Polyzois Makras. "Bone metabolism in Langerhans cell histiocytosis." Endocrine Connections 7, no. 7 (July 2018): R246—R253. http://dx.doi.org/10.1530/ec-18-0186.

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Langerhans cell histiocytosis (LCH) is a rare disease of not well-defined etiology that involves immune cell activation and frequently affects the skeleton. Bone involvement in LCH usually presents in the form of osteolytic lesions along with low bone mineral density. Various molecules involved in bone metabolism are implicated in the pathogenesis of LCH or may be affected during the course of the disease, including interleukins (ILs), tumor necrosis factor α, receptor activator of NF-κB (RANK) and its soluble ligand RANKL, osteoprotegerin (OPG), periostin and sclerostin. Among them IL-17A, pe

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Omata, Yasunori, Michael Frech, Taku Saito, Georg Schett, Mario M. Zaiss, and Sakae Tanaka. "Inflammatory Arthritis and Bone Metabolism Regulated by Type 2 Innate and Adaptive Immunity." International Journal of Molecular Sciences 23, no. 3 (January 20, 2022): 1104. http://dx.doi.org/10.3390/ijms23031104.

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While type 2 immunity has traditionally been associated with the control of parasitic infections and allergic reactions, increasing evidence suggests that type 2 immunity exerts regulatory functions on inflammatory diseases such as arthritis, and also on bone homeostasis. This review summarizes the current evidence of the regulatory role of type 2 immunity in arthritis and bone. Key type 2 cytokines, like interleukin (IL)-4 and IL-13, but also others such as IL-5, IL-9, IL-25, and IL-33, exert regulatory properties on arthritis, dampening inflammation and inducing resolution of joint swelling.

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Imai, K., M. W. Neuman, T. Kawase, and S. Saito. "Calcium in osteoblast-enriched bone cells." Bone 13, no. 3 (May 1992): 217–23. http://dx.doi.org/10.1016/8756-3282(92)90200-g.

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Montjovent, Marc-Olivier, Nathalie Burri, Silke Mark, Ermanno Federici, Corinne Scaletta, Pierre-Yves Zambelli, Patrick Hohlfeld, Pierre-François Leyvraz, Lee L. Applegate, and Dominique P. Pioletti. "Fetal bone cells for tissue engineering." Bone 35, no. 6 (December 2004): 1323–33. http://dx.doi.org/10.1016/j.bone.2004.07.001.

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Schett, G. "T and B cells and bone." Bone 48 (May 2011): S56—S57. http://dx.doi.org/10.1016/j.bone.2011.03.030.

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