osteopontin and bone

However, analysis of chimera mice with competitive reconstitution of WT and IRF8-KO bone marrow cells as well as mice with IRF8 deficiency only in T cells indicated that IRF8 plays no intrinsic role in CTL activation. Review articles are excluded from this waiver policy. β2M levels … As expected, the functions of OPN in the bone have become a research hotspot. Studies have shown that OPN plays a role in bone metabolism and homeostasis. Thus, all these mechanisms may represent a crosstalk between adipose tissue and skeleton, detrimental for bone health. Osteopontin (OPN) is a multifunctional protein mainly associated with bone metabolism and remodeling. Clipboard, Search History, and several other advanced features are temporarily unavailable. These are principally osteopontin (bone sialoprotein), matrix glutamic acid rich (GLA) protein, and the closely related osteocalcin, osteonectin, and proteoglycans (biglycans). Deletion of OPN in BSP knockout mice does not correct bone hypomineralization but results in high bone turnover.  |  Epub 2015 Jun 27. OPN not only is an important factor in neuron-mediated and endocrine-regulated bone mass, but also is involved in biological activities such as proliferation, migration, and adhesion of several bone-related cells, including bone marrow mesenchymal stem cells, hematopoietic stem cells, osteoclasts, and osteoblasts. Molecular mechanisms of adipocyte differentiation have been studied using both in vitro and in vivo models but the cellular and molecular mechanisms mediating the pathological switch in fat remain to be determined [39]. Adipose tissues are the major source of OPN and also of its obesity-induced upregulation. In addition, experimental and epidemiological evidence emerging disclosed complex cytokine and hormonal crosstalk between bone cells, liver, and adipose tissue, which adjusts coordinated bone remodeling, energy metabolism, and glucose homeostasis; changes in this network may contribute to the pathogenesis of obesity and related disorders [58], but some key questions have not yet been resolved. 2015 Dec;81:7-15. doi: 10.1016/j.bone.2015.05.047. AD is a chronic neurodegenerative disease and is the cause of 60% to 70% of cases of dementia [15–18]. Adipokines influence bone remodeling (obesity of bone) through upregulated proinflammatory cytokine production and exert an indirect effect on the sympathetic tone via hypothalamic nuclei. Several roles have been ascribed to osteopontin in bone, many of which have the potential to impact material properties. Besides its physiological functions, OPN is implicated in the pathogenesis of a variety of disease states, such as obesity and osteoporosis. Di Bernardo et al. At bone level, OPN has multifaceted effects on morphogenesis and remodeling [3, 6, 13, 14], being associated with bone turnover and bone mineral density (BMD). Triggiani and colleagues [30], too, have observed similar results. De Luca, “Resting energy expenditure and fat-free mass do not decline during aging in severely obese women,”, G. Messina, A. Viggiano, D. Tafuri et al., “Role of orexin in obese patients in the intensive care unit,”, K.-C. Kim, D.-H. Shin, S.-Y. Many researchers considered osteoporosis as a faultiness of bone marrow MSCs [74] in differentiating into other cell lineages, with adipogenesis being enhanced compared to osteoblastogenesis. Originally described by Senger in 1979 as a secreted, 60-kDa transformation-specific phosphoprotein [8], human OPN is the most studied component of SIBLING family. OPN, a multifunctional protein, is considered crucial for bone remodeling, biomineralization, and periodontal remodeling during mechanical tension and stress (orthodontic tooth movement). • Spp1 knockout in mice causes increased volumes and densities of dentin and alveolar bone • An imbalance has been described between normal adipogenesis and osteogenesis of MSCs, prevailing adipocyte differentiation on osteoblast differentiation [67]. OPN has a gly-arg-gly-asp-ser (GRGDS) [9] cell binding domain with ~314 amino acid residues that can regulate cell activities through integrin receptors. Copyright © 2017 Carolina De Fusco et al. OPN was identified in 1980; it is a key regulator of many metabolic and inflammatory diseases, such as diabetes, cardiovascular disease, and obesity. Osteopontin (OPN) is one of the major non-collagen proteins in extracellular bone matrix. -, Mckee MD, Nanci A. Osteopontin: An interfacial extracellular matrix protein in mineralized tissues. It is encoded by the SPP1 gene, which maps to the long arm of chromosome 4 [6] as a tandem array and generates three splice variants of mRNA, including the isoforms OPN-A, OPN-B, and OPN-C. OPN-A constitutes the full-length variant [2], whereas isoforms B (missing exon 5) and C (missing exon 4) are the splice variants [1, 2]. Connect Tissue Res. OPN is produced by cells located in the osteoid matrix, and its name “osteopontin” denotes the property of acting as a bridge (“pons” in Latin) between cells and hydroxyapatite of bone [2, 6]. Some studies have shown that OPN is causally involved in the pathogenesis of insulin resistance and type 2 diabetes, while other studies have shown that OPN is a protective islet protein preserving insulin secretion. These modifications give them bioactive properties [7]. Expression array studies on human adipose tissue have pointed out an activation of several inflammatory pathways in obesity [46]. Lee, J.-A. In vitro studies suggest that Opn and vascular endothelial growth factor (VEGF) cooperatively enhance angiogenesis in MM [2,3]. Luo, “Transdifferentiation between bone and fat on bone metabolism,”, M. Esposito, F. P. Serpe, G. Diletti et al., “Serum levels of polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans and polychlorinated biphenyls in a population living in the Naples area, southern Italy,”, A. Viggiano, U. Nicodemo, E. Viggiano et al., “Mastication overload causes an increase in O2- production into the subnucleus oralis of the spinal trigeminal nucleus,”, B. Rinaldi, F. Guida, A. Furiano et al., “Effect of prolonged moderate exercise on the changes of nonneuronal cells in early myocardial infarction,”, G. Di Bernardo, G. Messina, S. Capasso et al., “Sera of overweight people promote in vitro adipocyte differentiation of bone marrow stromal cells,”. -. J Clin Med. Differentiation. Osteopontin (OPN) is a highly phosphorylated sialoprotein that is a prominent component of the mineralized extracellular matrices of bones and teeth. [45] have demonstrated that postmenopausal women have more than twice bone marrow fat compared with premenopausal women. NIH  |  These data point toward a specific pathophysiological role of OPN in obesity. The presence of OPN in various organs, including those with and without matrix, and also in plasma, suggests that this molecule could act both as a structural molecule and as a humoral factor, or cytokine. [73]. Osteopontin (OPN), also defined as secreted phosphoprotein-1 [1] (SPP1), sialoprotein-1 [1, 2], or early T lymphocyte activation 1 (Eta-1) [3] belongs to the small integrin-binding ligand N-linked glycoprotein (SIBLING) family [4]. A quantitative study of 84 iliac bone biopsies,”, C. Rozman, E. Feliu, L. Berga, J.-C. Reverter, C. Climent, and M.-J. Proteolytic processing of osteopontin by PHEX and accumulation of osteopontin fragments in Hyp mouse bone, the murine model of X-linked hypophosphatemia. Bone sialoprotein and osteopontin in bone metastasis of osteotropic cancers. Different theories have been proposed to explain the complex interplay between adipose tissue and bone [16, 17]. In mouse models and obese humans, OPN is one of many inflammatory molecules overexpressed in adipose tissue [60, 61]. To elucidate the function of OPN in bone metabolism, a cellular defect was created in parietal bone and tibia of 12 rats. Foster BL(1), Ao M(2), Salmon CR(3), Chavez MB(4), Kolli TN(4), Tran AB(2), Chu EY(2), Kantovitz KR(5), Yadav M(6), Narisawa S(6), Millán JL(6), Nociti FH Jr(3), Somerman MJ(2). Osteocalcin is a 49-amino acid bone matrix noncollagen protein produced by osteoblasts, which is involved in bone deposition and calcium homeostasis. Background Osteopontin (OPN) has been implicated in bone remodeling by activating the resorption process. HHS A. de Paula, M. C. Horowitz, and C. J. Rosen, “Novel insights into the relationship between diabetes and osteoporosis,”, F. W. Kiefer, M. Zeyda, K. Gollinger et al., “Neutralization of osteopontin inhibits obesity-induced inflammation and insulin resistance,”, M. Kawai, F. J. Im, and D.-C. Lee, “Relation between obesity and bone mineral density and vertebral fractures in Korean postmenopausal women,”, A. Cohen, D. W. Dempster, R. R. Recker et al., “Abdominal fat is associated with lower bone formation and inferior bone quality in healthy premenopausal women: a transiliac bone biopsy study,”, E. A. Greco, D. Francomano, R. Fornari et al., “Negative association between trunk fat, insulin resistance and skeleton in obese women,”, E. F. Papakitsou, A. N. Margioris, K. E. Dretakis et al., “Body mass index (BMI) and parameters of bone formation and resorption in postmenopausal women,”, F. Wannenes, V. Papa, E. A. Greco et al., “Abdominal fat and sarcopenia in women significantly alter osteoblasts homeostasis in vitro by a WNT/, L. da Silva Meirelles, P. C. Chagastelles, and N. B. Nardi, “Mesenchymal stem cells reside in virtually all post-natal organs and tissues,”, T. Akune, S. Ohba, S. Kamekura et al., “PPAR, C. M. Digirolamo, D. Stokes, D. Colter, D. G. Phinney, R. Class, and D. J. Prockop, “Propagation and senescence of human marrow stromal cells in culture: a simple colony-forming assay identifies samples with the greatest potential to propagate and differentiate,”, T. Takahashi, “Overexpression of Runx2 and MKP-1 stimulates transdifferentiation of 3T3-L1 preadipocytes into bone-forming osteoblasts in vitro,”, D. K. W. Yeung, J. F. Griffith, G. E. Antonio, F. K. H. Lee, J. 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