Journal articles: 'Bone anabolism'

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Ruan, Feng, Qiang Zheng, and Jinfu Wang. "Mechanisms of bone anabolism regulated by statins." Bioscience Reports 32, no. 6 (September 14, 2012): 511–19. http://dx.doi.org/10.1042/bsr20110118.

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Osteoporosis is a common disease in the elderly population. The progress of this disease results in the reduction of bone mass and can increase the incidence of fractures. Drugs presently used clinically can block the aggravation of this disease. However, these drugs cannot increase the bone mass and may result in certain side effects. Statins, also known as HMG-CoA (3-hydroxy-3-methylglutaryl-CoA) reductase inhibitors, have been widely prescribed for CVD (cardiovascular disease) for decades. Nonetheless, several studies have demonstrated that statins exert bone anabolic effect and may be helpful for the treatment of osteoporosis. Several experiments have analysed the mechanisms of bone anabolism regulated by statins. In the present paper, we review the mechanisms of promoting osteogenesis, suppressing osteoblast apoptosis and inhibiting osteoclastogenesis.

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Martin, T. "Uncoupling anabolism from bone resorption." Bone 44 (June 2009): S203. http://dx.doi.org/10.1016/j.bone.2009.03.016.

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Hariri, Hadla, Martin Pellicelli, and René St-Arnaud. "New PTH Signals Mediating Bone Anabolism." Current Molecular Biology Reports 3, no. 2 (April 22, 2017): 133–41. http://dx.doi.org/10.1007/s40610-017-0060-z.

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Klein, Gordon L. "The Role of Bone in Muscle Wasting." International Journal of Molecular Sciences 22, no. 1 (December 31, 2020): 392. http://dx.doi.org/10.3390/ijms22010392.

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This review describes the role of bone resorption in muscle atrophy as well as in muscle protein anabolism. Both catabolic and anabolic pathways involve components of the proinflammatory cytokine families and release of factors stored in bone during resorption. The juxtaposition of the catabolic and anabolic resorption-dependent pathways raises new questions about control of release of factors from bone, quantity of release in a variety of conditions, and relation of factors released from bone. The catabolic responses involve release of calcium from bone into the circulation resulting in increased inflammatory response in intensity and/or duration. The release of transforming growth factor beta (TGF-β) from bone suppresses phosphorylation of the AKT/mTOR pathway and stimulates ubiquitin-mediated breakdown of muscle protein. In contrast, muscle IL-6 production is stimulated by undercarboxylated osteocalcin, which signals osteoblasts to produce more RANK ligand, stimulating resorptive release of undercarboxylated osteocalcin, which in turn stimulates muscle fiber nutrient uptake and an increase in muscle mass.

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Tu, Xiaolin, Jesus Delgado-Calle, Keith W. Condon, Marta Maycas, Huajia Zhang, Nadia Carlesso, Makoto M. Taketo, David B. Burr, Lilian I. Plotkin, and Teresita Bellido. "Osteocytes mediate the anabolic actions of canonical Wnt/β-catenin signaling in bone." Proceedings of the National Academy of Sciences 112, no. 5 (January 20, 2015): E478—E486. http://dx.doi.org/10.1073/pnas.1409857112.

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Osteocytes, >90% of the cells in bone, lie embedded within the mineralized matrix and coordinate osteoclast and osteoblast activity on bone surfaces by mechanisms still unclear. Bone anabolic stimuli activate Wnt signaling, and human mutations of components along this pathway underscore its crucial role in bone accrual and maintenance. However, the cell responsible for orchestrating Wnt anabolic actions has remained elusive. We show herein that activation of canonical Wnt signaling exclusively in osteocytes [dominant active (da)βcatOt mice] induces bone anabolism and triggers Notch signaling without affecting survival. These features contrast with those of mice expressing the same daß-catenin in osteoblasts, which exhibit decreased resorption and perinatal death from leukemia. daßcatOt mice exhibit increased bone mineral density in the axial and appendicular skeleton, and marked increase in bone volume in cancellous/trabecular and cortical compartments compared with littermate controls. daßcatOt mice display increased resorption and formation markers, high number of osteoclasts and osteoblasts in cancellous and cortical bone, increased bone matrix production, and markedly elevated periosteal bone formation rate. Wnt and Notch signaling target genes, osteoblast and osteocyte markers, and proosteoclastogenic and antiosteoclastogenic cytokines are elevated in bones of daßcatOt mice. Further, the increase in RANKL depends on Sost/sclerostin. Thus, activation of osteocytic β-catenin signaling increases both osteoclasts and osteoblasts, leading to bone gain, and is sufficient to activate the Notch pathway. These findings demonstrate disparate outcomes of β-catenin activation in osteocytes versus osteoblasts and identify osteocytes as central target cells of the anabolic actions of canonical Wnt/β-catenin signaling in bone.

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Horcajada, Marie-Noelle, and Elizabeth Offord. "Naturally Plant-Derived Compounds: Role in Bone Anabolism." Current Molecular Pharmacology 5, no. 2 (May 1, 2012): 205–18. http://dx.doi.org/10.2174/1874467211205020205.

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Kramer, Ina, Hansjoerg Keller, Olivier Leupin, and Michaela Kneissel. "Does osteocytic SOST suppression mediate PTH bone anabolism?" Trends in Endocrinology & Metabolism 21, no. 4 (April 2010): 237–44. http://dx.doi.org/10.1016/j.tem.2009.12.002.

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Torre, Elisa. "Molecular signaling mechanisms behind polyphenol-induced bone anabolism." Phytochemistry Reviews 16, no. 6 (August 31, 2017): 1183–226. http://dx.doi.org/10.1007/s11101-017-9529-x.

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Cheng, Su-Li, Jian-Su Shao, Jun Cai, Oscar L. Sierra, and Dwight A. Towler. "Msx2 Exerts Bone Anabolism via Canonical Wnt Signaling." Journal of Biological Chemistry 283, no. 29 (May 15, 2008): 20505–22. http://dx.doi.org/10.1074/jbc.m800851200.

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Towler, Dwight A. "Skeletal anabolism, PTH, and the bone-vascular axis." Journal of Bone and Mineral Research 26, no. 11 (October 21, 2011): 2579–82. http://dx.doi.org/10.1002/jbmr.523.

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GALLANT, MAXIME A., ESTELLE CHAMOUX, MARTINE BISSON, CATARINA WOLSEN, JEAN-LUC PARENT, SOPHIE ROUX, and ARTUR J. de BRUM-FERNANDES. "Increased Concentrations of Prostaglandin D2 During Post-Fracture Bone Remodeling." Journal of Rheumatology 37, no. 3 (January 15, 2010): 644–49. http://dx.doi.org/10.3899/jrheum.090622.

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Objective.To test the hypothesis that increased concentrations of prostaglandin D2 (PGD2) correlate with bone remodeling. Studies using isolated bone cells indicate that PGD2 may be implicated in the regulation of bone homeostasis, with a positive influence on bone anabolism. We studied patients with traumatic fractures and age- and sex-matched healthy controls as an in vivo model of increased bone remodeling.Methods.Thirty-five patients with bone fracture and matched controls were recruited. Urine and sera samples were collected. Urinary 11ß-PGF2α, a PGD2 metabolite, and PGE2 metabolites (PGEM), serum lipocalin-type PGD2 synthase (L-PGDS), bone alkaline phosphatase (bone ALP), and crosslinked C-telopeptides of type I collagen (CTX) were measured.Results.At 5–6 weeks post-fracture, 11ß-PGF2α, L-PGDS, bone ALP, and CTX were significantly increased in the fracture patients compared to controls. PGEM levels were not different between groups. Levels of 11ß-PGF2α and bone ALP were positively correlated, suggesting that PGD2 may be implicated in fracture repair.Conclusion.These results support our working hypothesis that PGD2 could be implicated in the control of bone anabolism in humans.

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Jilka, Robert L. "Inhibiting the Inhibitor: A New Route to Bone Anabolism." Journal of Bone and Mineral Research 24, no. 4 (April 2009): 575–77. http://dx.doi.org/10.1359/jbmr.090228.

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Brazill, Jennifer M., Alec T. Beeve, Clarissa S. Craft, Jason J. Ivanusic, and Erica L. Scheller. "Nerves in Bone: Evolving Concepts in Pain and Anabolism." Journal of Bone and Mineral Research 34, no. 8 (July 26, 2019): 1393–406. http://dx.doi.org/10.1002/jbmr.3822.

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Zaloszyc, Ariane, Claus Peter Schmitt, Amira Sayeh, Laetitia Higel, Catherine-Isabelle Gros, Fabien Bornert, Gaëlle Aubertin-Kirch, et al. "Frequent, quantitative bone planar scintigraphy for determination of bone anabolism in growing mice." PeerJ 9 (December 9, 2021): e12355. http://dx.doi.org/10.7717/peerj.12355.

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Background To provide insight into bone turnover, quantitative measurements of bone remodeling are required. Radionuclide studies are widely used in clinical care, but have been rarely used in the exploration of the bone in preclinical studies. We describe a bone planar scintigraphy method for frequent assessment of bone activity in mice across the growing period. Since repeated venous radiotracer injections are hardly feasible in mice, we investigated the subcutaneous route. Methods Repeated 99mTc-hydroxymethylene diphosphonate (HMDP) tracer bone planar scintigraphy studies of the knee region and µCT to measure femur growth rate were performed in eight mice between week 6 and week 27 of life, i.e., during their growth period. Three independent investigators assessed the regions of interest (ROI). An index was calculated based on the counts in knees ROI (normalized by pixels and seconds), corrected for the activity administered, the decay between administration and imaging, and individual weights. Results A total of 93 scintigraphy studies and 85 µCT were performed. Repeated subcutaneous tracer injections were well tolerated and allowed for adequate radionuclide studies. Mean scintigraphic indexes in the knees ROI decreased from 87.4 ± 2.6 × 10−6 counts s−1 pixel−1 MBq−1 g−1 at week 6 to 15.0 ± 3.3 × 10−6 counts s−1 pixel−1 MBq−1 g−1 at week 27. The time constant of the fitted exponential decay was equal to 23.5 days. As control mean femur length assessed by µCT increased from 12.2 ± 0.8 mm at week 6 to 15.8 ± 0.2 mm at week 22. The time constant of the fitted Gompertz law was equal to 26.7 days. A correlation index of −0.97 was found between femur growth and decrease of bone tracer activity count between week 6 and 24. Conclusion This methodological study demonstrates the potential of repeated bone planar scintigraphy in growing mice, with subcutaneous route for tracer administration, for quantitative assessment of bone remodeling.

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Stegen, Steve, Sophie Torrekens, Riet Van Looveren, Peter Carmeliet, and Geert Carmeliet. "Glutamine metabolism in osteoprogenitors governs bone mass accrual and PTH-induced bone anabolism." Bone Reports 13 (October 2020): 100661. http://dx.doi.org/10.1016/j.bonr.2020.100661.

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Wang, Feng-Sheng, Re-Wen Wu, Yu-Shan Chen, Jih-Yang Ko, Holger Jahr, and Wei-Shiung Lian. "Biophysical Modulation of the Mitochondrial Metabolism and Redox in Bone Homeostasis and Osteoporosis: How Biophysics Converts into Bioenergetics." Antioxidants 10, no. 9 (August 30, 2021): 1394. http://dx.doi.org/10.3390/antiox10091394.

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Bone-forming cells build mineralized microstructure and couple with bone-resorbing cells, harmonizing bone mineral acquisition, and remodeling to maintain bone mass homeostasis. Mitochondrial glycolysis and oxidative phosphorylation pathways together with ROS generation meet the energy requirement for bone-forming cell growth and differentiation, respectively. Moderate mechanical stimulations, such as weight loading, physical activity, ultrasound, vibration, and electromagnetic field stimulation, etc., are advantageous to bone-forming cell activity, promoting bone anabolism to compromise osteoporosis development. A plethora of molecules, including ion channels, integrins, focal adhesion kinases, and myokines, are mechanosensitive and transduce mechanical stimuli into intercellular signaling, regulating growth, mineralized extracellular matrix biosynthesis, and resorption. Mechanical stimulation changes mitochondrial respiration, biogenesis, dynamics, calcium influx, and redox, whereas mechanical disuse induces mitochondrial dysfunction and oxidative stress, which aggravates bone-forming cell apoptosis, senescence, and dysfunction. The control of the mitochondrial biogenesis activator PGC-1α by NAD+-dependent deacetylase sirtuins or myokine FNDC/irisin or repression of oxidative stress by mitochondrial antioxidant Nrf2 modulates the biophysical stimulation for the promotion of bone integrity. This review sheds light onto the roles of mechanosensitive signaling, mitochondrial dynamics, and antioxidants in mediating the anabolic effects of biophysical stimulation to bone tissue and highlights the remedial potential of mitochondrial biogenesis regulators for osteoporosis.

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Robling, Alexander G., Rajendra Kedlaya, Shana N. Ellis, Paul J. Childress, Joseph P. Bidwell, Teresita Bellido, and Charles H. Turner. "Anabolic and Catabolic Regimens of Human Parathyroid Hormone 1–34 Elicit Bone- and Envelope-Specific Attenuation of Skeletal Effects in Sost-Deficient Mice." Endocrinology 152, no. 8 (June 7, 2011): 2963–75. http://dx.doi.org/10.1210/en.2011-0049.

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PTH is a potent calcium-regulating factor that has skeletal anabolic effects when administered intermittently or catabolic effects when maintained at consistently high levels. Bone cells express PTH receptors, but the cellular responses to PTH in bone are incompletely understood. Wnt signaling has recently been implicated in the osteo-anabolic response to the hormone. Specifically, the Sost gene, a major antagonist of Wnt signaling, is down-regulated by PTH exposure. We investigated this mechanism by treating Sost-deficient mice and their wild-type littermates with anabolic and catabolic regimens of PTH and measuring the skeletal responses. Male Sost+/+ and Sost−/− mice were injected daily with human PTH 1–34 (0, 30, or 90 μg/kg) for 6 wk. Female Sost+/+ and Sost−/− mice were continuously infused with vehicle or high-dose PTH (40 μg/kg · d) for 3 wk. Dual energy x-ray absorptiometry-derived measures of intermittent PTH (iPTH)-induced bone gain were impaired in Sost−/− mice. Further probing revealed normal or enhanced iPTH-induced cortical bone formation rates but concomitant increases in cortical porosity among Sost−/− mice. Distal femur trabecular bone was highly responsive to iPTH in Sost−/− mice. Continuous PTH (cPTH) infusion resulted in equal bone loss in Sost+/+ and Sost−/− mice as measured by dual energy x-ray absorptiometry. However, distal femur trabecular bone, but not lumbar spine trabecular bone, was spared the bone-wasting effects of cPTH in Sost−/− mice. These results suggest that changes in Sost expression are not required for iPTH-induced anabolism. iPTH-induced resorption of cortical bone might be overstimulated in Sost-deficient environments. Furthermore, Sost deletion protects some trabecular compartments, but not cortical compartments, from bone loss induced by high-dose PTH infusion.

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Negri, Stefano, T. Jake Samuel, and Seungyong Lee. "The Potential Role of Exercise Training and Mechanical Loading on Bone-Associated Skeletal Nerves." Journal of Bone Metabolism 28, no. 4 (November 30, 2021): 267–77. http://dx.doi.org/10.11005/jbm.2021.28.4.267.

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The spatial distribution, innervation, and functional role of the bone-associated skeletal nerves have been previously reported in detail. However, studies examining exercise-induced associations between skeletal nerves and bone metabolism are limited. This review introduces a potential relationship between exercise and the skeletal nerves and discusses how it can contribute to exercise-induced bone anabolism. First, the background and current understanding of nerve fiber types and their functions in the skeleton are provided. Next, the influence of exercise and mechanical loading on the skeletal nervous system is elaborated. Effective synthesis of recent studies could serve as an established baseline for the novel discovery of the effects of exercise on skeletal nerve density and bone anabolic activity in the future. Therefore, this review overviews the existing evidence for the neural control of bone metabolism and the potential positive effects of exercise on the peripheral skeletal nervous system. The influence of exercise training models on the relationships of sensory nerve signals with osteoblast-mediated bone formation and the increased bone volume provides the first insight on the potential importance of exercise training in stimulating positive adaptations in the skeletal nerve-bone interaction and its downstream effect on bone metabolism, thereby highlighting its therapeutic potential in a variety of clinical populations.

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Kramer, Ina, Gabriela G. Loots, and Michaela Kneissel. "PTH-induced bone anabolism is blunted in SOST overexpressing mice." Bone 42 (March 2008): S56—S57. http://dx.doi.org/10.1016/j.bone.2007.12.098.

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Alloisio, Giulia, Chiara Ciaccio, Giovanni Francesco Fasciglione, Umberto Tarantino, Stefano Marini, Massimo Coletta, and Magda Gioia. "Effects of Extracellular Osteoanabolic Agents on the Endogenous Response of Osteoblastic Cells." Cells 10, no. 9 (September 10, 2021): 2383. http://dx.doi.org/10.3390/cells10092383.

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The complex multidimensional skeletal organization can adapt its structure in accordance with external contexts, demonstrating excellent self-renewal capacity. Thus, optimal extracellular environmental properties are critical for bone regeneration and inextricably linked to the mechanical and biological states of bone. It is interesting to note that the microstructure of bone depends not only on genetic determinants (which control the bone remodeling loop through autocrine and paracrine signals) but also, more importantly, on the continuous response of cells to external mechanical cues. In particular, bone cells sense mechanical signals such as shear, tensile, loading and vibration, and once activated, they react by regulating bone anabolism. Although several specific surrounding conditions needed for osteoblast cells to specifically augment bone formation have been empirically discovered, most of the underlying biomechanical cellular processes underneath remain largely unknown. Nevertheless, exogenous stimuli of endogenous osteogenesis can be applied to promote the mineral apposition rate, bone formation, bone mass and bone strength, as well as expediting fracture repair and bone regeneration. The following review summarizes the latest studies related to the proliferation and differentiation of osteoblastic cells, enhanced by mechanical forces or supplemental signaling factors (such as trace metals, nutraceuticals, vitamins and exosomes), providing a thorough overview of the exogenous osteogenic agents which can be exploited to modulate and influence the mechanically induced anabolism of bone. Furthermore, this review aims to discuss the emerging role of extracellular stimuli in skeletal metabolism as well as their potential roles and provide new perspectives for the treatment of bone disorders.

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Pignolo, Robert. "COP Cells in States of Bone Anabolism and Abnormal Calciﬁcation/Ossification." Innovation in Aging 5, Supplement_1 (December 1, 2021): 45. http://dx.doi.org/10.1093/geroni/igab046.169.

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Abstract Circulating osteogenic progenitor (COP) cells are a population of cells in the peripheral blood with the capacity for bone formation, as well as broader differentiation into mesoderm-like cells in vitro. There are several pathologies of accelerated bone formation and physiological responses to injury in which COP cells have been theorized to play a role. These include fracture, vascular calciﬁcation, and subtypes of heterotopic ossiﬁcation (HO). Overall, the available studies suggest COP cells are likely to be mobilized in response to fracture, home to the site of injury, undergo a maturation process, and contribute to the osteogenesis and angiogenesis required for fracture healing. HO is the pathological process of bone formation in nonskeletal tissue and can be acquired or hereditary. COP cells may seed sites of injury and inﬂammation that precede the formation of endochondral bone identiﬁed in both genetic and nongenetic forms of HO. Vascular calciﬁcation is a common occurrence in older adults and is strongly associated with poorer cardiovascular health outcomes. It appears that COP cells, particularly those expressing hematopoietic and vascular markers such as CD45 and CD34, contribute to the calciﬁcation and ossification of atherosclerotic plaques and aortic valves, and that they correlate to the severity of the calciﬁcation. Whether COP cells are attracted to sites of injury and inﬂammation and so are highly associated with fracture, vascular calcification/ossification and HO, or whether they underlie these processes at a more mechanistic level, remains to be more clearly demonstrated.

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Karner, Courtney M., Emel Esen, Adewole L. Okunade, Bruce W. Patterson, and Fanxin Long. "Increased glutamine catabolism mediates bone anabolism in response to WNT signaling." Journal of Clinical Investigation 125, no. 2 (December 22, 2014): 551–62. http://dx.doi.org/10.1172/jci78470.

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Aslan, Yetki, Lea Hanna Doumit Sakr, Judith Luce, Sylvie Thomasseau, Rafailia Vakasiri, Claire-Sophie Devignes, and Sylvain Provot. "PTH-induced bone anabolism promotes systemic breast cancer growth and metastasis." Bone Reports 13 (October 2020): 100332. http://dx.doi.org/10.1016/j.bonr.2020.100332.

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Esen, Emel, Seung-Yon Lee, Burton M. Wice, and Fanxin Long. "PTH Promotes Bone Anabolism by Stimulating Aerobic Glycolysis via IGF Signaling." Journal of Bone and Mineral Research 30, no. 11 (July 14, 2015): 1959–68. http://dx.doi.org/10.1002/jbmr.2556.

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Esen, Emel, Seung-Yon Lee, Burton M. Wice, and Fanxin Long. "PTH Promotes Bone Anabolism by Stimulating Aerobic Glycolysis via IGF Signaling." Journal of Bone and Mineral Research 30, no. 11 (October 19, 2015): 2137. http://dx.doi.org/10.1002/jbmr.2714.

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Sage, Andrew P., Jinxiu Lu, Elisa Atti, Sotirios Tetradis, Maria-Grazia Ascenzi, Douglas J. Adams, Linda L. Demer, and Yin Tintut. "Hyperlipidemia induces resistance to PTH bone anabolism in mice via oxidized lipids." Journal of Bone and Mineral Research 26, no. 6 (May 24, 2011): 1197–206. http://dx.doi.org/10.1002/jbmr.312.

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van Niekerk, Gustav, Megan Mitchell, and Anna-Mart Engelbrecht. "Bone resorption: supporting immunometabolism." Biology Letters 14, no. 2 (February 2018): 20170783. http://dx.doi.org/10.1098/rsbl.2017.0783.

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Activation of the immune system is associated with an increase in the breakdown of various peripheral tissues, including bone. Despite the widely appreciated role of inflammatory mediators in promoting bone resorption, the functional value behind this process is not completely understood. Recent advances in the field of immunometabolism have highlighted the metabolic reprogramming that takes place in activated immune cells. It is now believed that the breakdown of peripheral tissue provides metabolic substrates to fuel metabolic anabolism in activated immune cells. We argue that phosphate, liberated by bone resorption, plays an indispensable role in sustaining immune cell metabolism. The liberated phosphate is then incorporated into macromolecules such as nucleotides and phospholipids, and is also used for the phosphorylation of metabolites (e.g. glycolytic intermediates). In addition, magnesium, also liberated during the breakdown of bone, is an essential cofactor required by various metabolic enzymes which are upregulated in activated immune cells. Finally, calcium activates various additional molecules involved in immune cell migration. Taken together, these factors suggest a key role for bone resorption during infection.

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Barbe, Mary F., Mamta Amin, Michele Y. Harris, Siva Tejaa Panibatla, Soroush Assari, Steven N. Popoff, and Geoffrey M. Bove. "Manual Therapy Facilitates Homeostatic Adaptation to Bone Microstructural Declines Induced by a Rat Model of Repetitive Forceful Task." International Journal of Molecular Sciences 23, no. 12 (June 13, 2022): 6586. http://dx.doi.org/10.3390/ijms23126586.

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The effectiveness of manual therapy in reducing the catabolic effects of performing repetitive intensive force tasks on bones has not been reported. We examined if manual therapy could reduce radial bone microstructural declines in adult female Sprague–Dawley rats performing a 12-week high-repetition and high-force task, with or without simultaneous manual therapy to forelimbs. Additional rats were provided 6 weeks of rest after task cessation, with or without manual therapy. The control rats were untreated or received manual therapy for 12 weeks. The untreated TASK rats showed increased catabolic indices in the radius (decreased trabecular bone volume and numbers, increased osteoclasts in these trabeculae, and mid-diaphyseal cortical bone thinning) and increased serum CTX-1, TNF-α, and muscle macrophages. In contrast, the TASK rats receiving manual therapy showed increased radial bone anabolism (increased trabecular bone volume and osteoblast numbers, decreased osteoclast numbers, and increased mid-diaphyseal total area and periosteal perimeter) and increased serum TNF-α and muscle macrophages. Rest, with or without manual therapy, improved the trabecular thickness and mid-diaphyseal cortical bone attributes but not the mineral density. Thus, preventive manual therapy reduced the net radial bone catabolism by increasing osteogenesis, while rest, with or without manual therapy, was less effective.

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Lei, Li, Li Meng, Xu Changqing, Zhu Chen, Yao Gang, and Fang Shiyuan. "Effect of cell receptors in the pathogenesis of osteoarthritis: Current insights." Open Life Sciences 17, no. 1 (January 1, 2022): 695–709. http://dx.doi.org/10.1515/biol-2022-0075.

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Abstract Osteoarthritis (OA) is a chronic arthritic disease characterized by cartilage degradation, synovial inflammation, and subchondral bone lesions. The studies on the pathogenesis of OA are complex and diverse. The roles of receptors signaling in chondrocyte anabolism, inflammatory factors expression of synovial fibroblast, and angiogenesis in subchondral bone are particularly important for exploring the pathological mechanism of OA and clinical diagnosis and treatment. By reviewing the relevant literature, this article elaborates on the abnormal expression of receptors and the signaling transduction pathways from different pathological changes of OA anatomical components, aiming to provide new research ideas and clinical therapeutic value for OA pathogenesis.

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Grant, Dale, David Tomlinson, Kostas Tsintzas, Petra Kolic, and Gladys Onambele-Pearson. "Displacing Sedentary Behaviour with Light Intensity Physical Activity Spontaneously Alters Habitual Macronutrient Intake and Enhances Dietary Quality in Older Females." Nutrients 12, no. 8 (August 13, 2020): 2431. http://dx.doi.org/10.3390/nu12082431.

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Displacing Sedentary Behaviour (SB) with light intensity physical activity (LIPA) is increasingly viewed as a viable means of health enhancement. It is, however, unclear whether any behavioural compensations accompany such an intervention. Therefore, the aim of this study was to identify any dietary changes that accompany SB displacement. We hypothesised that SB displacement would improve dietary quality. Thirty-five elderly females (73 ± 5 years) were randomly allocated to one of three groups: (1) sedentary behaviour fragmentation (SBF) (n = 14), (2) continuous LIPA (n = 14), or (3) control (n = 7). Habitual diet (four-day food diary) and physical behaviour (accelerometery) were assessed at weeks 0 and 8. Out of 45 nutrients examined, only glucose exhibited a group × time interaction (p = 0.03), mediated by an exclusive reduction following SBF (−31%). SBF was also the sole experimental group to increase nutrients promoting bone health (SBF: 17%, LIPA: −34%. control: 21%), whereas both experimental groups consumed more nutrients promoting anabolism (SBF: 13%, LIPA: 4%, control: −34%) (z-scores). New ambulators (n = 8) also consumed more nutrients promoting bone health (16%)/anabolism (2%) (z-scores), including significantly increased Zinc intake (p = 0.05, 29%). Displacing SB with LIPA improves dietary quality in older females. Furthermore, SB fragmentation appears advantageous for various dietary outcomes.

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Rhee, Yumie, Eun-Young Lee, Virginia Lezcano, Ana C. Ronda, Keith W. Condon, Matthew R. Allen, Lilian I. Plotkin, and Teresita Bellido. "Resorption Controls Bone Anabolism Driven by Parathyroid Hormone (PTH) Receptor Signaling in Osteocytes." Journal of Biological Chemistry 288, no. 41 (August 20, 2013): 29809–20. http://dx.doi.org/10.1074/jbc.m113.485938.

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Lu, Chien-Lin, Jia-Fwu Shyu, Chia-Chao Wu, Chi-Feng Hung, Min-Tser Liao, Wen-Chih Liu, Cai-Mei Zheng, Yi-Chou Hou, Yuh-Feng Lin, and Kuo-Cheng Lu. "Association of Anabolic Effect of Calcitriol with Osteoclast-Derived Wnt 10b Secretion." Nutrients 10, no. 9 (August 25, 2018): 1164. http://dx.doi.org/10.3390/nu10091164.

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Canonical Wnt (Wingless/Integrated) signaling is crucial in bone development and the Wnt ligand can promote osteoblast differentiation from mesenchymal progenitor cells. Calcitriol, an active vitamin D3, is used clinically for treatment of secondary hyperparathyroidism (SHPT) in chronic kidney disease (CKD) patients. The bone effects of calcitriol in SHPT remains uncertain. We hypothesized that calcitriol improves bone mass by suppressing osteoclast activity, and simultaneously promoting Wnt ligand secretion. We designed a cross-sectional study in maintenance hemodialysis patients to explore the effects of calcitriol on different bone turnover markers and specifically emphasized the Wnt 10b levels. Then, we explored the source of Wnt 10b secretion by using osteoclasts and osteoblasts treated with calcitriol in cell culture studies. Finally, we explored the effects of calcitriol on bone microarchitectures in CKD mice, using the 5/6 nephrectomy CKD animal model with analysis using micro-computed tomography. Calcitriol promoted the growth of both trabecular and cortical bones in the CKD mice. Wnt 10b and Procollagen 1 N-terminal Propeptide (P1NP) significantly increased, but Tartrate-resistant acid phosphatase 5b (Trap 5b) significantly decreased in the calcitriol-treated maintenance hemodialysis patients. Calcitriol enhanced Wnt 10b secretion from osteoclasts in a dose-dependent manner. Treatment of SHPT with calcitriol improved the bone anabolism by inhibiting osteoclasts and promoting osteoblasts that might be achieved by increasing the Wnt 10b level.

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Kot, Alexander, Zhendong A. Zhong, Hongliang Zhang, Yu-An Evan Lay, Nancy E. Lane, and Wei Yao. "Sex dimorphic regulation of osteoprogenitor progesterone in bone stromal cells." Journal of Molecular Endocrinology 59, no. 4 (November 2017): 351–63. http://dx.doi.org/10.1530/jme-17-0076.

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Increasing peak bone mass is a promising strategy to prevent osteoporosis. A mouse model of global progesterone receptor (PR) ablation showed increased bone mass through a sex-dependent mechanism. Cre-Lox recombination was used to generate a mouse model of osteoprogenitor-specific PR inactivation, which recapitulated the high bone mass phenotype seen in the PR global knockout mouse mode. In this work, we employed RNA sequencing analysis to evaluate sex-independent and sex-dependent differences in gene transcription of osteoprogenitors of wild-type and PR conditional knockout mice. PR deletion caused marked sex hormone-dependent changes in gene transcription in male mice as compared to wild-type controls. These transcriptional differences revealed dysregulation in pathways involving immunomodulation, osteoclasts, bone anabolism, extracellular matrix interaction and matrix interaction. These results identified many potential mechanisms that may explain our observed high bone mass phenotype with sex differences when PR was selectively deleted in the MSCs.

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Kamiya, Nobuhiro. "The Role of BMPs in Bone Anabolism and their Potential Targets SOST and DKK1." Current Molecular Pharmacology 5, no. 2 (May 1, 2012): 153–63. http://dx.doi.org/10.2174/1874467211205020153.

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Corrigan, Michele A., Siobhan Coyle, Kian F. Eichholz, Mathieu Riffault, Brian Lenehan, and David A. Hoey. "Aged Osteoporotic Bone Marrow Stromal Cells Demonstrate Defective Recruitment, Mechanosensitivity, and Matrix Deposition." Cells Tissues Organs 207, no. 2 (2019): 83–96. http://dx.doi.org/10.1159/000503444.

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Bone formation requires the replenishment of the osteoblast from a progenitor or stem cell population, which must be recruited, expanded, and differentiated to ensure continued anabolism. How this occurs and whether it is altered in the osteoporotic environment is poorly understood. Furthermore, given that emerging treatments for osteoporosis are targeting this progenitor population, it is critical to determine the regenerative capacity of this cell type in the setting of osteoporosis. Human bone marrow stromal cells (hMSCs) from a cohort of aged osteoporotic patients were compared to MSCs isolated from healthy donors in terms of the ability to undergo recruitment and proliferation, and also respond to both the biophysical and biochemical cues that drive osteogenic matrix deposition. hMSCs isolated from healthy donors demonstrate good recruitment, mechanosensitivity, proliferation, and differentiation capacity. Contrastingly, hMSCs isolated from aged osteoporotic patients had significantly diminished regenerative potential. Interestingly, we demonstrated that osteoporotic hMSCs no longer responded to chemokine-directing recruitment and became desensitised to mechanical stimulation. The osteoporotic MSCs had a reduced proliferative potential and, importantly, they demonstrated an attenuated differentiation capability with reduced mineral and lipid formation. Moreover, during osteogenesis, despite minimal differences in the quantity of deposited collagen, the distribution of collagen was dramatically altered in osteoporosis, suggesting a potential defect in matrix quality. Taken together, this study has demonstrated that hMSCs isolated from aged osteoporotic patients demonstrate defective cell behaviour on multiple fronts, resulting in a significantly reduced regenerative potential, which must be considered during the development of new anabolic therapies that target this cell population.

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Sadchikov, P. E., I. L. Goldman, S. V. Razin, A. D. Chernousov, L. I. Alekseeva, and E. R. Sadchikova. "THE MOLECULAR MECHANISM OF LACTOFERRIN INFLUENCE ON BONE FORMATION." Osteoporosis and Bone Diseases 19, no. 3 (December 15, 2016): 12–22. http://dx.doi.org/10.14341/osteo2016312-22.

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In present critical review of systematized materials on the breakthrough achievements of the last decade - the discovery of the effect of protein lactoferrin (LF) on bone formation. It is shownthat LF increases the number of osteoblasts, stimulate their proliferation and differentiation, and prevents their destruction. Action of LF exceeds that of many other previously established bone-forming factors. LF increases the ability of osteoblasts to synthesize and mineralize bone matrix. Apparently, the effect of LF on bone anabolism ensured by the presence of specific receptors on osteoblasts. It was found that LF also inhibits the formation of osteoclasts. Experimental studies have demonstrated that LF prevents the destruction of bone tissue in ovariectomizedanimals and, thus, developing the type of postmenstrual osteoporosis in women. We get the first clinical studies demonstrating an increase in the period of healing of bone injuries while reducing the level of endogenous LF. Since molecular research establishes that the expression of the LF gene is regulated by estrogen, which reduces the development of postmenopausal osteoporosis (PMO) in women, there is a need to further investigate the relationship of these processes, which will help to create a basis for the management of bone formation.

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Yu, Yaling, Shujie Wang, and Zhenlei Zhou. "Cartilage Homeostasis Affects Femoral Head Necrosis Induced by Methylprednisolone in Broilers." International Journal of Molecular Sciences 21, no. 14 (July 8, 2020): 4841. http://dx.doi.org/10.3390/ijms21144841.

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(1) Background: Since the large-scale poultry industry has been established, femoral head necrosis (FHN) has always been a major leg disease in fast-growing broilers worldwide. Previous research suggested that cartilage homeostasis could be taken into consideration in the cause of FHN, but the evidence is insufficient. (2) Methods: One-day-old broiler chickens were randomly divided into three groups, 16 broilers per group. The birds in group L were injected intramuscularly with methylprednisolone (MP) twice a week for four weeks (12.5 mg·kg−1). The birds in group H were injected intramuscularly with MP (20 mg·kg−1·d−1) for 7 d (impulse treatment). The birds in group C were treated with sterile saline as a control group. Broilers were sacrificed at 42 and 56 d. Blood samples were collected from the jugular vein for ELISA and biochemical analysis. Bone samples, including femur, tibia, and humerus, were collected for histopathological analysis, bone parameters detection, and real-time quantitative PCR detection. (3) Results: The FHN broilers in group L and H both showed lower body weight (BW) and reduced bone parameters. In addition, the MP treatment resulted in reduced extracellular matrix (ECM) anabolism and enhanced ECM catabolism. Meanwhile, the autophagy and apoptosis of chondrocytes were enhanced, which led to the destruction of cartilage homeostasis. Moreover, the impulse MP injection increased the portion of birds with severer FHN, whereas the MP injection over a long period caused a more evident change in serum cytokine concentrations and bone metabolism indicators. (4) Conclusions: The imbalance of cartilage homeostasis may play a critical role in the development of FHN in broilers. FHN broilers induced by MP showed a more pronounced production of catabolic factors and suppressed the anabolic factors, which might activate the genes of the WNT signal pathway and hypoxia-inducible factors (HIFs), and then upregulate the transcription expression of ECM to restore homeostasis.

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Barbe, Mary F., Vicky S. Massicotte, Soroush Assari, Nagat Frara, Michele Y. Harris, Mamta Amin, Tamara King, Geneva E. Cruz, and Steve N. Popoff. "Prolonged high force high repetition pulling induces trabecular bone loss and microcracks, while low force high repetition pulling induces bone anabolism." Proceedings of the Human Factors and Ergonomics Society Annual Meeting 62, no. 1 (September 2018): 813–17. http://dx.doi.org/10.1177/1541931218621186.

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We have an operant rat model of upper extremity reaching and grasping in which we examined the impact of performing a high force high repetition (High-ForceHR) versus a low force low repetition (Low-ForceHR) task for 18 weeks on the radius, compared to age-matched controls. High-ForceHR rats performed at 4 reaches/min and 50% of their maximum voluntary pulling force for 2 hrs/day, 3 days/wk. Low-ForceHR rats performed at 6% maximum voluntary pulling force. High-ForceHR rats showed decreased trabecular bone volume in the distal radius and increased catabolic indices (microcracks and increased osteocyte apoptosis), compared to controls. In contrast, Low-ForceHR rats showed increased trabecular bone volume, and no microcracks or osteocyte apoptosis. Thus, prolonged performance of an upper extremity reaching and grasping task is loading-dependent with high force loading leading to accumulation of bone microdamage. The target grasp force (1.27N) of the High-ForceHR rats was 50% of their mean maximum voluntary force of 2.45N, easily below the predicted maximum acceptable force (MAF) of 1.64N (predicted from published equations). The presence of microcracks and bone loss leads us to suggest that the published equations over-estimated the MAF on these tissues by 1.3 fold.

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Rennie, M. J. "Exercise- and nutrient-controlled mechanisms involved in maintenance of the musculoskeletal mass." Biochemical Society Transactions 35, no. 5 (October 25, 2007): 1302–5. http://dx.doi.org/10.1042/bst0351302.

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The mechanisms of maintenance of the protein mass of muscle and associated connective tissue and bone are becoming more accessible as a result of the use of a combination of well-established techniques for measurement of protein turnover and measurement of protein expression and phosphorylation state of signalling molecules involved in anabolic and catabolic responses. Amino acids, hormones and physical activity appear to be the major short-term physiological regulators of muscle mass, mainly through their actions on protein synthesis and breakdown, on a time scale of minutes to hours, with duration of changes in gene expression up to weeks. Amino acids are the main components in the diet regulating protein turnover, having marked effects in stimulating muscle protein synthesis and with almost no effect on muscle protein breakdown. Branched-chain amino acids, and in particular leucine, simulate protein synthesis via signalling pathways involving mTOR (mammalian target of rapamycin) in a dose–response manner. Insulin has little effect on protein synthesis in human muscle, but it has a marked inhibitory effect on protein breakdown. The amino acid simulation of anabolism is not dependent on the presence of insulin, IGF-1 (insulin-like growth factor-1) or growth hormone. Exercise not only stimulates protein synthesis in muscle, but also in tendon; and disuse atrophy is accompanied by marked decreases of both muscle and tendon collagen protein synthesis. Bone collagen synthesis appears to be nutritionally regulated by the availability of amino acids, but not lipid or glucose.

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Imai, Shinji, and Yoshitaka Matsusue. "Neuronal regulation of bone metabolism and anabolism: Calcitonin gene-related peptide-, substance P-, and tyrosine hydroxylase-containing nerves and the bone." Microscopy Research and Technique 58, no. 2 (July 15, 2002): 61–69. http://dx.doi.org/10.1002/jemt.10119.

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Ardeshirpour, Laleh, Pamela Dann, Douglas J. Adams, Tracey Nelson, Joshua VanHouten, Mark C. Horowitz, and John J. Wysolmerski. "Weaning Triggers a Decrease in Receptor Activator of Nuclear Factor-κB Ligand Expression, Widespread Osteoclast Apoptosis, and Rapid Recovery of Bone Mass after Lactation in Mice." Endocrinology 148, no. 8 (August 1, 2007): 3875–86. http://dx.doi.org/10.1210/en.2006-1467.

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A significant portion of milk calcium comes from the mother’s skeleton, and lactation is characterized by rapid bone loss. The most remarkable aspect of this bone loss is its complete reversibility, and the time after weaning is the most rapid period of skeletal anabolism in adults. Despite this, little is known of the mechanisms by which the skeleton repairs itself after lactation. We examined changes in bone and calcium metabolism defining the transition from bone loss to bone recovery at weaning in mice. Bone mass decreases during lactation and recovers rapidly after weaning. Lactation causes changes in bone microarchitecture, including thinning and perforation of trabecular plates that are quickly repaired after weaning. Weaning causes a rapid decline in urinary C-telopeptide levels and stimulates an increase in circulating levels of osteocalcin. Bone histomorphometry documented a significant reduction in the numbers of osteoclasts on d 3 after weaning caused by a coordinated wave of osteoclast apoptosis beginning 48 h after pup removal. In contrast, osteoblast numbers and bone formation rates, which are elevated during lactation, remain so 3 d after weaning. The cessation of lactation stimulates an increase in circulating calcium levels and a reciprocal decrease in PTH levels. Finally, weaning is associated with a decrease in levels of receptor activator of nuclear factor-κB ligand mRNA in bone. In conclusion, during lactation, bone turnover is elevated, and bone loss is rapid. Weaning causes selective apoptosis of osteoclasts halting bone resorption. The sudden shift in bone turnover favoring bone formation subsequently contributes to the rapid recovery of bone mass.

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Gentile, Michael A., Pascale V. Nantermet, Robert L. Vogel, Robert Phillips, Daniel Holder, Paul Hodor, Chun Cheng, Hongyue Dai, Leonard P. Freedman, and William J. Ray. "Androgen-mediated improvement of body composition and muscle function involves a novel early transcriptional program including IGF1, mechano growth factor, and induction of β-catenin." Journal of Molecular Endocrinology 44, no. 1 (September 1, 2009): 55–73. http://dx.doi.org/10.1677/jme-09-0048.

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Androgens promote anabolism in the musculoskeletal system while generally repressing adiposity, leading to lean body composition. Circulating androgens decline with age, contributing to frailty, osteoporosis, and obesity; however, the mechanisms by which androgens modulate body composition are largely unknown. Here, we demonstrate that aged castrated rats develop increased fat mass, reduced muscle mass and strength, and lower bone mass. Treatment with testosterone or 5α-dihydrotestosterone (DHT) reverses the effects on muscle and adipose tissues while only aromatizable testosterone increased bone mass. During the first week, DHT transiently increased soleus muscle nuclear density and induced expression of IGF1 and its splice variant mechano growth factor (MGF) without early regulation of the myogenic factors MyoD, myogenin, monocyte nuclear factor, or myostatin. A genome-wide microarray screen was also performed to identify potential pro-myogenic genes that respond to androgen receptor activation in vivo within 24 h. Of 24 000 genes examined, 70 candidate genes were identified whose functions suggest initiation of remodeling and regeneration, including the type II muscle genes for myosin heavy chain type II and parvalbumin and the chemokine monocyte chemoattractant protein-1. Interestingly, Axin and Axin2, negative regulators of β-catenin, were repressed, indicating modulation of the β-catenin pathway. DHT increased total levels of β-catenin protein, which accumulated in nuclei in vivo. Likewise, treatment of C2C12 myoblasts with both IGF1Ea and MGF C-terminal peptide increased nuclear β-catenin in vitro. Thus, we propose that androgenic anabolism involves early downregulation of Axin and induction of IGF1, leading to nuclear accumulation of β-catenin, a pro-myogenic, anti-adipogenic stem cell regulatory factor.

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Mansouri, Rafik, Yohann Jouan, Eric Hay, Claudine Blin-Wakkach, Monique Frain, Agnès Ostertag, Carole Le Henaff, et al. "Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells." Cell Death & Disease 8, no. 6 (June 2017): e2902-e2902. http://dx.doi.org/10.1038/cddis.2017.287.

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Abstract Stimulating bone formation is an important challenge for bone anabolism in osteoporotic patients or to repair bone defects. The osteogenic properties of matrix glycosaminoglycans (GAGs) have been explored; however, the functions of GAGs at the surface of bone-forming cells are less documented. Syndecan-2 is a membrane heparan sulfate proteoglycan that is associated with osteoblastic differentiation. We used a transgenic mouse model with high syndecan-2 expression in osteoblasts to enrich the bone surface with cellular GAGs. Bone mass was increased in these transgenic mice. Syndecan-2 overexpression reduced the expression of receptor activator of NF-kB ligand (RANKL) in bone marrow cells and strongly inhibited bone resorption. Osteoblast activity was not modified in the transgenic mice, but bone formation was decreased in 4-month-old transgenic mice because of reduced osteoblast number. Increased proteoglycan expression at the bone surface resulted in decreased osteoblastic and osteoclastic precursors in bone marrow. Indeed, syndecan-2 overexpression increased apoptosis of mesenchymal precursors within the bone marrow. However, syndecan-2 specifically promoted the vasculature characterized by high expression of CD31 and Endomucin in 6-week-old transgenic mice, but this was reduced in 12-week-old transgenic mice. Finally, syndecan-2 functions as an inhibitor of Wnt-β-catenin–T-cell factor signaling pathway, activating glycogen synthase kinase 3 and then decreasing the Wnt-dependent production of Wnt ligands and R-spondin. In conclusion, our results show that GAG supply may improve osteogenesis, but also interfere with the crosstalk between the bone surface and marrow cells, altering the supporting function of osteoblasts.

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Sequetto, Priscila L., Reggiani V. Gonçalves, Aloísio S. Pinto, Maria G. A. Oliveira, Izabel R. S. C. Maldonado, Tânia T. Oliveira, and Rômulo D. Novaes. "Low Doses of Simvastatin Potentiate the Effect of Sodium Alendronate in Inhibiting Bone Resorption and Restore Microstructural and Mechanical Bone Properties in Glucocorticoid-Induced Osteoporosis." Microscopy and Microanalysis 23, no. 5 (July 26, 2017): 989–1001. http://dx.doi.org/10.1017/s1431927617012363.

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AbstractBy using an experimental model of dexamethasone-induced osteoporosis we investigated the effects of different therapeutic schemes combining sodium alendronate (SA) and simvastatin on bone mineral and protein composition, microstructural and mechanical remodeling. Wistar rats were randomized into eight groups: G1: non-osteoporotic; G2: osteoporotic; G3, G4, and G5: osteoporotic+SA (0.2, 0.4, and 0.8 mg/kg, respectively); G6, G7, and G8: osteoporotic+SA (0.2, 0.4, and 0.8 mg/kg, respectively)+simvastatin (0.4, 0.6, and 1 mg/kg, respectively). Osteoporosis was induced by dexamethasone (7 mg/kg, i.m.) once a week for 5 weeks. All treatments were administered for 8 weeks. Dexamethasone increased serum levels of alkaline phosphatase, calcium, phosphorus, and urea, especially in non-treated animals, which showed severe osteoporosis. Dexamethasone also induced bone microstructural fragility and reduced mechanical resistance, which were associated with a marked depletion in mineral mass, collagenous and non-collagenous protein levels in cortical and cancellous bone. Although SA has attenuated osteoporosis severity, the effectiveness of drug therapy was enhanced combining alendronate and simvastatin. The restoration in serum parameters, organic and inorganic bone mass, and mechanical behavior showed a dose-dependent effect that was potentially related to the complementary mechanisms by which each drug acts to induce bone anabolism, accelerating tissue repair.

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Lian, Wei-Shiung, Re-Wen Wu, Yu-Shan Chen, Jih-Yang Ko, Shao-Yu Wang, Holger Jahr, and Feng-Sheng Wang. "MicroRNA-29a in Osteoblasts Represses High-Fat Diet-Mediated Osteoporosis and Body Adiposis through Targeting Leptin." International Journal of Molecular Sciences 22, no. 17 (August 24, 2021): 9135. http://dx.doi.org/10.3390/ijms22179135.

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Skeletal tissue involves systemic adipose tissue metabolism and energy expenditure. MicroRNA signaling controls high-fat diet (HFD)-induced bone and fat homeostasis dysregulation remains uncertain. This study revealed that transgenic overexpression of miR-29a under control of osteocalcin promoter in osteoblasts (miR-29aTg) attenuated HFD-mediated body overweight, hyperglycemia, and hypercholesterolemia. HFD-fed miR-29aTg mice showed less bone mass loss, fatty marrow, and visceral fat mass together with increased subscapular brown fat mass than HFD-fed wild-type mice. HFD-induced O2 underconsumption, respiratory quotient repression, and heat underproduction were attenuated in miR-29aTg mice. In vitro, miR-29a overexpression repressed transcriptomic landscapes of the adipocytokine signaling pathway, fatty acid metabolism, and lipid transport, etc., of bone marrow mesenchymal progenitor cells. Forced miR-29a expression promoted osteogenic differentiation but inhibited adipocyte formation. miR-29a signaling promoted brown/beige adipocyte markers Ucp-1, Pgc-1α, P2rx5, and Pat2 expression and inhibited white adipocyte markers Tcf21 and Hoxc9 expression. The microRNA also reduced peroxisome formation and leptin expression during adipocyte formation and downregulated HFD-induced leptin expression in bone tissue. Taken together, miR-29a controlled leptin signaling and brown/beige adipocyte formation of osteogenic progenitor cells to preserve bone anabolism, which reversed HFD-induced energy underutilization and visceral fat overproduction. This study sheds light on a new molecular mechanism by which bone integrity counteracts HFD-induced whole-body fat overproduction.

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Yu, Yaling, Lishan Lin, Kangping Liu, Yixin Jiang, and Zhenlei Zhou. "Effects of Simvastatin on Cartilage Homeostasis in Steroid-Induced Osteonecrosis of Femoral Head by Inhibiting Glucocorticoid Receptor." Cells 11, no. 24 (December 7, 2022): 3945. http://dx.doi.org/10.3390/cells11243945.

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Steroid-induced osteonecrosis of femoral head (SONFH) is one of the most common bone disorders in humans. Statin treatment is beneficial in preventing the development of SONFH through anti-inflammation effects and inhibition of the glucocorticoid receptor (GR). However, potential mechanisms of statin action remain to be determined. In this study, pulse methylprednisolone (MP) treatment was used to induce SONFH in broilers, and then MP-treated birds were administrated with simvastatin simultaneously to investigate the changes in cartilage homeostasis. Meanwhile, chondrocytes were isolated, cultured, and treated with MP, simvastatin, or GR inhibitor in vitro. The changes in serum homeostasis factors, cell viability, and expression of GR were analyzed. The results showed that the morbidity of SONFH in the MP-treated group increased significantly compared with the simvastatin-treated and control group. Furthermore, MP treatment induced apoptosis and high-level catabolism and low-level anabolism in vitro and vivo, while simvastatin significantly decreased catabolism and slightly recovered anabolism via inhibiting GR and the hypoxia-inducible factor (HIF) pathway. The GR inhibitor or its siRNA mainly affected the catabolism of cartilage homeostasis in vitro. In conclusion, the occurrence of SONFH in broilers was related to the activation of GR and HIF pathway, and imbalance of cartilage homeostasis. Simvastatin and GR inhibitor maintained cartilage homeostasis via GR and the HIF pathway.

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Ko, Jih-Yang, Feng-Sheng Wang, Sung-Hsiung Chen, Re-Wen Wu, Chieh-Cheng Hsu, and Shu-Jui Kuo. "The Antagonism of Neuropeptide Y Type I Receptor (Y1R) Reserves the Viability of Bone Marrow Stromal Cells in the Milieu of Osteonecrosis of Femoral Head (ONFH)." Biomedicines 10, no. 11 (November 15, 2022): 2942. http://dx.doi.org/10.3390/biomedicines10112942.

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Neuropeptide Y (NPY)-Y1 receptor (Y1R) signaling is known to negatively affect bone anabolism. Our study aimed at investigating the impact of NPY-Y1R signaling in the pathogenesis of glucocorticoid-related osteonecrosis of the femoral head (ONFH). Femoral heads were retrieved from 20 patients with and without ONFH, respectively. The bone marrow stromal cells (BMSCs) from ONFH femoral heads were treated with Y1R agonists and antagonists for subsequent analysis. We showed that the local NPY expression level was lower in ONFH heads. The Y1R agonists and antagonists disturb and facilitate the survival of BMSCs. The transcription of stromal derived factor-1 (SDF-1) was enhanced by Y1R antagonists. Our study showed that the local NPY expression level was lower in ONFH heads. Y1R antagonists facilitate the survival of BMSCs and stimulate the transcription of SDF-1 by BMSCs. These findings shed light on the role of NPY-Y1R signaling in the pathogenesis of ONFH.

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Shao, Yu, Emily Wichern, Paul J. Childress, Michele Adaway, Jagannath Misra, Angela Klunk, David B. Burr, et al. "Loss of Nmp4 optimizes osteogenic metabolism and secretion to enhance bone quality." American Journal of Physiology-Endocrinology and Metabolism 316, no. 5 (May 1, 2019): E749—E772. http://dx.doi.org/10.1152/ajpendo.00343.2018.

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A goal of osteoporosis therapy is to restore lost bone with structurally sound tissue. Mice lacking the transcription factor nuclear matrix protein 4 ( Nmp4, Zfp384, Ciz, ZNF384) respond to several classes of osteoporosis drugs with enhanced bone formation compared with wild-type (WT) animals. Nmp4−/− mesenchymal stem/progenitor cells (MSPCs) exhibit an accelerated and enhanced mineralization during osteoblast differentiation. To address the mechanisms underlying this hyperanabolic phenotype, we carried out RNA-sequencing and molecular and cellular analyses of WT and Nmp4−/− MSPCs during osteogenesis to define pathways and mechanisms associated with elevated matrix production. We determined that Nmp4 has a broad impact on the transcriptome during osteogenic differentiation, contributing to the expression of over 5,000 genes. Phenotypic anchoring of transcriptional data was performed for the hypothesis-testing arm through analysis of cell metabolism, protein synthesis and secretion, and bone material properties. Mechanistic studies confirmed that Nmp4−/− MSPCs exhibited an enhanced capacity for glycolytic conversion: a key step in bone anabolism. Nmp4−/− cells showed elevated collagen translation and secretion. The expression of matrix genes that contribute to bone material-level mechanical properties was elevated in Nmp4−/− cells, an observation that was supported by biomechanical testing of bone samples from Nmp4−/− and WT mice. We conclude that loss of Nmp4 increases the magnitude of glycolysis upon the metabolic switch, which fuels the conversion of the osteoblast into a super-secretor of matrix resulting in more bone with improvements in intrinsic quality.

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Wu, Jun, Rong Wang, Xuechun Kan, Jinghan Zhang, Wen Sun, David Goltzman, and Dengshun Miao. "A Sonic Hedgehog-Gli-Bmi1 signaling pathway plays a critical role in p27 deficiency induced bone anabolism." International Journal of Biological Sciences 18, no. 3 (2022): 956–69. http://dx.doi.org/10.7150/ijbs.65954.

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Cai, J., W. Li, T. Sun, X. Li, E. Luo, and D. Jing. "Pulsed electromagnetic fields preserve bone architecture and mechanical properties and stimulate porous implant osseointegration by promoting bone anabolism in type 1 diabetic rabbits." Osteoporosis International 29, no. 5 (March 9, 2018): 1177–91. http://dx.doi.org/10.1007/s00198-018-4392-1.

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Journal articles on the topic 'Bone anabolism'

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