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Status: Bibliographieeintrag

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Verfasst von:Kawelke, Nina [VerfasserIn]   i
 Bentmann, Anke [VerfasserIn]   i
 Hackl, Norman J. [VerfasserIn]   i
 Hager, Hans-Dieter [VerfasserIn]   i
 Feick, Peter [VerfasserIn]   i
 Geursen, Anne [VerfasserIn]   i
 Singer, Manfred V. [VerfasserIn]   i
 Nakchbandi, Inaam [VerfasserIn]   i
Titel:Isoform of fibronectin mediates bone loss in patients with primary biliary cirrhosis by suppressing bone formation
Verf.angabe:Nina Kawelke, Anke Bentmann, Norman Hackl, Hans-Dieter Hager, Peter Feick, Anne Geursen, Manfred V. Singer, and Inaam A. Nakchbandi
E-Jahr:2008
Jahr:March 17, 2008
Umfang:9 S.
Fussnoten:Gesehen am 30.06.2021
Titel Quelle:Enthalten in: Journal of bone and mineral research
Ort Quelle:[Oxford] : Oxford University Press, 1986
Jahr Quelle:2008
Band/Heft Quelle:23(2008), 8, Seite 1278-1286
ISSN Quelle:1523-4681
Abstract:Osteoporosis is a major cause of morbidity and decreased quality of life in patients with chronic cholestatic liver disease. It is established that this osteoporosis results from decreased bone formation, but the mechanisms for the interaction between liver and bone remain elusive. The aim of this study was to test the hypothesis that an increase in the production of cellular fibronectins during liver disease may result in decreased osteoblast-mediated mineralization and thus explain the decrease in bone formation. We performed a prospective cross-sectional study in patients with primary biliary cirrhosis and matched controls, followed by experiments on human and mouse osteoblasts in culture and injections in mice in vivo. In patients with primary biliary cirrhosis, the oncofetal domain of fibronectin correlated significantly with the decrease in osteocalcin, a marker of bone formation (r = -0.57, p < 0.05). In vitro, amniotic fluid fibronectin (aFN) containing mainly the oncofetal domain and EIIIA domain resulted in decreased osteoblast-mediated mineralization in human osteoblasts (69% decrease at 100 microg/ml; p < 0.01) and mouse osteoblasts (71% decrease; p < 0.05). Removing the EIIIA domain from aFN similarly suppressed mineralization by osteoblasts (78% decrease; p < 0.05). Injection of labeled aFN in mice showed that it infiltrates the bone, and its administration over 10 days resulted in decreased trabecular BMD (17% drop; p < 0.05), mineralizing surface (30% drop; p < 0.005), and number of osteoblasts (45% drop; p < 0.05). Increased production of a fibronectin isoform containing the oncofetal domain and its release in the circulation in patients with primary biliary cirrhosis is at least partially responsible for the decrease in bone formation seen in these patients. This establishes that a molecule that has thus far been viewed as an extracellular matrix protein exerts hormone-like actions.
DOI:doi:10.1359/jbmr.080313
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: https://doi.org/10.1359/jbmr.080313
 Volltext: https://asbmr.onlinelibrary.wiley.com/doi/full/10.1359/jbmr.080313
 DOI: https://doi.org/10.1359/jbmr.080313
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:Amniotic Fluid
 Animals
 Biomarkers
 Bone Density
 Bone Resorption
 Calcification, Physiologic
 Cells, Cultured
 Female
 Fibronectins
 Humans
 Injections, Intraperitoneal
 Liver Cirrhosis, Biliary
 Male
 Mice
 Middle Aged
 Osteoblasts
 Osteocalcin
 Osteogenesis
 Protein Isoforms
 Tibia
K10plus-PPN:1761588494
Verknüpfungen:→ Zeitschrift

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