8
views
0
recommends
+1 Recommend
1 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Influencia de la regucalcina en la pérdida de masa ósea Translated title: Influence of regucalcin on bone loss

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Resumen Objetivo. El propósito de este trabajo ha sido revisar la literatura científica con relación al papel de la regucalcina en la pérdida de masa ósea. Método. Se realizó una búsqueda bibliográfica en la base de datos PubMed. Se encontraron 31 artículos. Tras analizar su contenido y aplicar los criterios de inclusión y exclusión, un total de 13 artículos fueron incluidos. Resultados. La disminución en el contenido de calcio femoral observado en ratones transgénicos con regucalcina se observó con el aumento de la edad, lo que sugiere que la pérdida ósea no se restaura con el modelado óseo. De la misma manera, se encontró que la adición de regucalcina con 1 a 100 nM estimulaba significativamente la actividad basal de NF-kB (P<0.01). Se apreció una disminución significativa en el contenido de ADN en los tejidos metafisarios femorales, con una mayor disminución en hembras que en machos, siendo estos valores: 3.3 mg/g pasaron a ser 2.6 mg/g en las hembras (P<0.01). La reabsorción ósea osteoclástica aumentó en ratones transgénicos con regucalcina machos y hembras con edad creciente. La regucalcina exógena revela efectos supresores sobre la osteoblastogénesis y la mineralización in vitro y que no tuvo efectos sobre la proliferación celular y la apoptosis en las células osteoblásticas en cultivos a corto plazo. Conclusión. La regucalcina desempeña un papel fundamental en el mantenimiento del homeostasis celular y la función de la respuesta celular en relación a la masa ósea.

          Translated abstract

          Abstract Purpose. The aim of this work has been to review the scientific literature regarding the role of regucalcin in bone loss. Method. A bibliographic search was performed in the PubMed database. A total of 31 articles were used. After analyzing its content and applying the inclusion and exclusion criteria, a total of 13 articles were included. Results The decrease in femoral calcium content observed in regucalcin transgenic mice decreased with increasing age, suggesting that bone loss is not restored with bone modeling. In the same way, it was found that the addition of regucalcin with 1 to 100 nM significantly stimulated the baseline activity of NF-kB (P <0.01). Likewise, there was a significant decrease in the DNA content in femoral metaphyseal tissues, with a greater decrease in females than in males, these values being: 3,3 mg / g became 2,6 mg / g (P <0.01). Osteoclastic bone resorption increased in male and female transgenic regucalcin mice with increasing age. Also, exogenous regucalcin reveals suppressive effects on osteoblastogenesis and mineralization in vitro and that it had no effects on cell proliferation and apoptosis in osteoblast cells in short-term cultures. Conclusion. Regucalcin plays a fundamental role in the maintenance of cell homeostasis and the function of the cellular response in relation to bone mass.

          Related collections

          Most cited references25

          • Record: found
          • Abstract: found
          • Article: not found

          Estrogen deficiency and bone loss: an inflammatory tale.

          Estrogen plays a fundamental role in skeletal growth and bone homeostasis in both men and women. Although remarkable progress has been made in our understanding of how estrogen deficiency causes bone loss, the mechanisms involved have proven to be complex and multifaceted. Although estrogen is established to have direct effects on bone cells, recent animal studies have identified additional unexpected regulatory effects of estrogen centered at the level of the adaptive immune response. Furthermore, a potential role for reactive oxygen species has now been identified in both humans and animals. One major challenge is the integration of a multitude of redundant pathways and cytokines, each apparently capable of playing a relevant role, into a comprehensive model of postmenopausal osteoporosis. This Review presents our current understanding of the process of estrogen deficiency-mediated bone destruction and explores some recent findings and hypotheses to explain estrogen action in bone. Due to the inherent difficulties associated with human investigation, many of the lessons learned have been in animal models. Consequently, many of these principles await further validation in humans.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The molecular understanding of osteoclast differentiation.

            Osteoclasts are multinucleated cells of monocyte/macrophage origin that degrade bone matrix. The differentiation of osteoclasts is dependent on a tumor necrosis factor (TNF) family cytokine, receptor activator of nuclear factor (NF)-kappaB ligand (RANKL), as well as macrophage colony-stimulating factor (M-CSF). Congenital lack of osteoclasts causes osteopetrosis, investigation of which has provided insights into the essential molecules for osteoclastogenesis, including TNF receptor-associated factor (TRAF) 6, NF-kappaB and c-Fos. In addition, genome-wide screening techniques have shed light on an additional set of gene products such as nuclear factor of activated T cells (NFAT) c1. Here we summarize the efforts to understand the sequential molecular events induced by RANKL during osteoclast differentiation. RANKL binds to its receptor RANK, which recruits adaptor molecules such as TRAF6. TRAF6 activates NF-kappaB, which is important for the initial induction of NFATc1. NFATc1 is activated by calcium signaling and binds to its own promoter, thus switching on an autoregulatory loop. An activator protein (AP)-1 complex containing c-Fos is required for the autoamplification of NFATc1, enabling the robust induction of NFATc1. Finally, NFATc1 cooperates with other transcriptional partners to activate osteoclast-specific genes. NFATc1 autoregulation is controlled by an epigenetic mechanism, which has profound implications for an understanding of the general mechanism of irreversible cell fate determination. From the clinical point of view, RANKL signaling pathway has promise as a strategy for suppressing the excessive osteoclast formation characteristic of a variety of bone diseases.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Senescence marker protein 30 functions as gluconolactonase in L-ascorbic acid biosynthesis, and its knockout mice are prone to scurvy.

              We originally identified senescence marker protein 30 (SMP30) as a distinctive protein whose expression decreases in an androgen-independent manner with aging. Here, we report its sequence homology found in two kinds of bacterial gluconolactonases (GNLs) by using the blast search. Then, through a biochemical study, we identify SMP30 as the lactone-hydrolyzing enzyme GNL of animal species. SMP30 purified from the rat liver had lactonase activity toward various aldonolactones, such as d- and l-glucono-delta-lactone, d- and l-gulono-gamma-lactone, and d- and l-galactono-gamma-lactone, with a requirement for Zn(2+) or Mn(2+) as a cofactor. Furthermore, in SMP30 knockout mice, no GNL activity was detectable in the liver. Thus, we conclude that SMP30 is a unique GNL in the liver. The lactonase reaction with l-gulono-gamma-lactone is the penultimate step in l-ascorbic acid (AA) biosynthesis, and the essential role of SMP30 in this synthetic process was verified here by a nutritional study using SMP30 knockout mice. These knockout mice (n = 6), fed a vitamin C-deficient diet, did not thrive; i.e., they displayed symptoms of scurvy such as bone fracture and rachitic rosary and then died by 135 days after the start of receiving the deficient diet. The AA levels in their livers and kidneys at the time of death were <1.6% of those in WT control mice. In addition, by using the SMP30 knockout mouse, we demonstrate that the alternative pathway of AA synthesis involving d-glucurono-gamma-lactone operates in vivo, although its flux is fairly small.
                Bookmark

                Author and article information

                Journal
                jonnpr
                Journal of Negative and No Positive Results
                JONNPR
                Research and Science S.L. (Madrid, Madrid, Spain )
                2529-850X
                2021
                : 6
                : 2
                : 232-243
                Affiliations
                [1] Cáceres Extremadura orgnameUniversidad de Extremadura orgdiv1Faculty of Sport Sciences orgdiv2Health, Economy, Motricity and Education Research Group Spain
                Article
                S2529-850X2021000200002 S2529-850X(21)00600200002
                10.19230/jonnpr.3650
                56f0e49a-08f1-4618-b92e-d202d5bda2cf

                This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.

                History
                : 20 March 2020
                : 13 August 2020
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 25, Pages: 12
                Product

                SciELO Spain

                Categories
                Original

                osteoclastos,osteoblastos,marcadores bioquímicos,contenido de calcio,SMP30,RGN,osteoblasts,osteoclasts,NF-kB,calcium content,biochemical markers,vía NF-kB

                Comments

                Comment on this article