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We are analyzing https://link.springer.com/article/10.1007/s00223-015-0013-6.

Title:
Biphasic Effects of Vitamin D and FGF23 on Human Osteoclast Biology | Calcified Tissue International
Description:
Vitamin D and FGF23 play a major role in calcium/phosphate balance. Vitamin D may control bone resorption but the potential role of FGF23 has never been evaluated. The objective of this study was therefore to compare the effects of vitamin D and FGF23 on osteoclast differentiation and activity in human monocyte-derived osteoclasts. Human monocytes, purified from blood of healthy donors, were incubated with M-CSF and RANKL to obtain mature multinucleated osteoclasts (MNC). Experiments were carried out to assess the effects of FGF23 as compared to native vitamin D (25-D) and active vitamin D (1,25-D) on osteoclast differentiation and on bone-resorbing osteoclast activity. Additional experiments with the pan fibroblast growth factor receptor inhibitor (FGFR-i) were performed. Phosphorylation Akt and Erk pathways were analyzed by Western blot analyses. Both 1,25-D and FGF23, to a lesser extent, significantly inhibited osteoclastogenesis at early stages; when adding FGFR-i, osteoclast formation was restored. Biochemical experiments showed an activation of the Akt and Erk pathways under FGF23 treatment. In contrast, in terms of activity, 1,25-D had no effect on resorption, whereas FGF23 slightly but significantly increased bone resorption; 25-D had no effects on either differentiation or on activity. These data show that 1,25-D inhibits osteoclastogenesis without regulating osteoclast-mediated bone resorption activity; FGF23 has biphasic effects on osteoclast physiology, inhibiting osteoclast formation while stimulating slightly osteoclast activity. These results may be of importance and taken into account in chronic kidney disease when therapies modulating FGF23 are available.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
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Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

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Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 7,625,932 visitors per month in the current month.

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How Does Link.springer.com Make Money? {💾}

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Not all websites are made for profit; some exist to inform or educate users. Or any other reason why people make websites. And this might be the case. Link.springer.com could have a money-making trick up its sleeve, but it's undetectable for now.

Keywords {🔍}

pubmed, article, google, scholar, cas, bone, fgf, central, osteoclast, human, vitamin, bacchetta, res, effects, differentiation, osteoclasts, fibroblast, growth, factor, miner, allard, justine, resorption, activity, clin, lyon, privacy, cookies, content, research, lise, machucagayet, osteoclastogenesis, kidney, phosphate, invest, wang, france, data, publish, search, tissue, demoncheaux, irma, georgess, fabienne, courylucas, role, experiments, access,

Topics {✒}

ifn-beta-dependent nfatc1 suppression month download article/chapter pÎle femme-mÚre-enfant fabienne coury-lucas mitogen-activated protein kinase justine bacchetta declare human monocyte-derived osteoclasts service de néphrologie serum phosphate-independent functions bone-resorbing osteoclast activity full article pdf control bone resorption chronic kidney disease systemic phosphate homeostasis master research project université de lyon justine bacchetta article allard calcium/phosphate balance human osteoclast biology privacy choices/manage cookies razzaque ms pereira rc wesseling-perry mineralized tissue cells pierre jurdic related subjects anti-osteoclastogenic action fgf23 transgenic mice c-fos protein irma machuca-gayet european economic area western blot analyses distal convoluted tubule rheumatoid arthritis microenvironment azucena-serrano ce inhibiting osteoclast formation renal phosphate transport significantly inhibited osteoclastogenesis kidney transplant loss therapies modulating fgf23 article log fgf23-mediated regulation conditions privacy policy accepting optional cookies klotho gene family acknowledge marlene mazzorana article cite osteoclast physiology biochemical experiments showed

Questions {❓}

  • Razzaque MS (2009) FGF23-mediated regulation of systemic phosphate homeostasis: is Klotho an essential player?

Schema {đŸ—ș}

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         description:Vitamin D and FGF23 play a major role in calcium/phosphate balance. Vitamin D may control bone resorption but the potential role of FGF23 has never been evaluated. The objective of this study was therefore to compare the effects of vitamin D and FGF23 on osteoclast differentiation and activity in human monocyte-derived osteoclasts. Human monocytes, purified from blood of healthy donors, were incubated with M-CSF and RANKL to obtain mature multinucleated osteoclasts (MNC). Experiments were carried out to assess the effects of FGF23 as compared to native vitamin D (25-D) and active vitamin D (1,25-D) on osteoclast differentiation and on bone-resorbing osteoclast activity. Additional experiments with the pan fibroblast growth factor receptor inhibitor (FGFR-i) were performed. Phosphorylation Akt and Erk pathways were analyzed by Western blot analyses. Both 1,25-D and FGF23, to a lesser extent, significantly inhibited osteoclastogenesis at early stages; when adding FGFR-i, osteoclast formation was restored. Biochemical experiments showed an activation of the Akt and Erk pathways under FGF23 treatment. In contrast, in terms of activity, 1,25-D had no effect on resorption, whereas FGF23 slightly but significantly increased bone resorption; 25-D had no effects on either differentiation or on activity. These data show that 1,25-D inhibits osteoclastogenesis without regulating osteoclast-mediated bone resorption activity; FGF23 has biphasic effects on osteoclast physiology, inhibiting osteoclast formation while stimulating slightly osteoclast activity. These results may be of importance and taken into account in chronic kidney disease when therapies modulating FGF23 are available.
         datePublished:2015-05-19T00:00:00Z
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      headline:Biphasic Effects of Vitamin D and FGF23 on Human Osteoclast Biology
      description:Vitamin D and FGF23 play a major role in calcium/phosphate balance. Vitamin D may control bone resorption but the potential role of FGF23 has never been evaluated. The objective of this study was therefore to compare the effects of vitamin D and FGF23 on osteoclast differentiation and activity in human monocyte-derived osteoclasts. Human monocytes, purified from blood of healthy donors, were incubated with M-CSF and RANKL to obtain mature multinucleated osteoclasts (MNC). Experiments were carried out to assess the effects of FGF23 as compared to native vitamin D (25-D) and active vitamin D (1,25-D) on osteoclast differentiation and on bone-resorbing osteoclast activity. Additional experiments with the pan fibroblast growth factor receptor inhibitor (FGFR-i) were performed. Phosphorylation Akt and Erk pathways were analyzed by Western blot analyses. Both 1,25-D and FGF23, to a lesser extent, significantly inhibited osteoclastogenesis at early stages; when adding FGFR-i, osteoclast formation was restored. Biochemical experiments showed an activation of the Akt and Erk pathways under FGF23 treatment. In contrast, in terms of activity, 1,25-D had no effect on resorption, whereas FGF23 slightly but significantly increased bone resorption; 25-D had no effects on either differentiation or on activity. These data show that 1,25-D inhibits osteoclastogenesis without regulating osteoclast-mediated bone resorption activity; FGF23 has biphasic effects on osteoclast physiology, inhibiting osteoclast formation while stimulating slightly osteoclast activity. These results may be of importance and taken into account in chronic kidney disease when therapies modulating FGF23 are available.
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         Differentiation
         FGF23
         Human
         Osteoclast
         Vitamin D
         Biochemistry
         general
         Endocrinology
         Orthopedics
         Cell Biology
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      name:Institut de GĂ©nomique Fonctionnelle de Lyon, ENS UMR 5242, UniversitĂ© de Lyon, Lyon, France
      name:Institut de GĂ©nomique Fonctionnelle de Lyon, ENS UMR 5242, UniversitĂ© de Lyon, Lyon, France
      name:INSERM 1033, Lyon, France
      name:Institut de GĂ©nomique Fonctionnelle de Lyon, ENS UMR 5242, UniversitĂ© de Lyon, Lyon, France
      name:Institut de GĂ©nomique Fonctionnelle de Lyon, ENS UMR 5242, UniversitĂ© de Lyon, Lyon, France
      name:INSERM 1033, Lyon, France
      name:Institut de GĂ©nomique Fonctionnelle de Lyon, ENS UMR 5242, UniversitĂ© de Lyon, Lyon, France
      name:Institut de GĂ©nomique Fonctionnelle de Lyon, ENS UMR 5242, UniversitĂ© de Lyon, Lyon, France
      name:INSERM 1033, Lyon, France
      name:Centre de RĂ©fĂ©rence des Maladies RĂ©nales Rares, Service de NĂ©phrologie et Rhumatologie PĂ©diatriques, Hospices Civils de Lyon, HĂŽpital Femme MĂšre Enfant, Bron Cedex, France
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