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<a href="http://doi.org/10.1016/j.ajpath.2013.11.031" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.ajpath.2013.11.031</a>
Pages
697–713
Issue
3
Volume
184
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Title
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Mutation in osteoactivin decreases bone formation in vivo and osteoblast differentiation in vitro.
Publisher
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The American journal of pathology
Date
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2014
2014-03
Subject
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*Signal Transduction; Alkaline Phosphatase/metabolism; Animals; Apoptosis; Bone and Bones/metabolism/pathology; Cell Differentiation/genetics; Eye Proteins/*genetics; Inbred DBA; Male; Membrane Glycoproteins/*genetics; Mice; Mutation; Newborn; Osteoblasts/cytology/*physiology; Osteocalcin/*genetics; Osteogenesis/*genetics; Phenotype; Receptors; Transforming Growth Factor beta/metabolism
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Abdelmagid Samir M; Belcher Joyce Y; Moussa Fouad M; Lababidi Suzanne L; Sondag Gregory R; Novak Kimberly M; Sanyurah Afif S; Frara Nagat A; Razmpour Roshanak; Del Carpio-Cano Fabiola E; Safadi Fayez F
Description
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We have previously identified osteoactivin (OA), encoded by Gpnmb, as an osteogenic factor that stimulates osteoblast differentiation in vitro. To elucidate the importance of OA in osteogenesis, we characterized the skeletal phenotype of a mouse model, DBA/2J (D2J) with a loss-of-function mutation in Gpnmb. Microtomography of D2J mice showed decreased trabecular mass, compared to that in wild-type mice [DBA/2J-Gpnmb(+)/SjJ (D2J/Gpnmb(+))]. Serum analysis showed decreases in OA and the bone-formation markers alkaline phosphatase and osteocalcin in D2J mice. Although D2J mice showed decreased osteoid and mineralization surfaces, their osteoblasts were increased in number, compared to D2J/Gpnmb(+) mice. We then examined the ability of D2J osteoblasts to differentiate in culture, where their differentiation and function were decreased, as evidenced by low alkaline phosphatase activity and matrix mineralization. Quantitative RT-PCR analyses confirmed the decreased expression of differentiation markers in D2J osteoblasts. In vitro, D2J osteoblasts proliferated and survived significantly less, compared to D2J/Gpnmb(+) osteoblasts. Next, we investigated whether mutant OA protein induces endoplasmic reticulum stress in D2J osteoblasts. Neither endoplasmic reticulum stress markers nor endoplasmic reticulum ultrastructure were altered in D2J osteoblasts. Finally, we assessed underlying mechanisms that might alter proliferation of D2J osteoblasts. Interestingly, TGF-beta receptors and Smad-2/3 phosphorylation were up-regulated in D2J osteoblasts, suggesting that OA contributes to TGF-beta signaling. These data confirm the anabolic role of OA in postnatal bone formation.
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<a href="http://doi.org/10.1016/j.ajpath.2013.11.031" target="_blank" rel="noreferrer noopener">10.1016/j.ajpath.2013.11.031</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Signal Transduction
2014
Abdelmagid Samir M
Alkaline Phosphatase/metabolism
Animals
Apoptosis
Belcher Joyce Y
Bone and Bones/metabolism/pathology
Cell Differentiation/genetics
Del Carpio-Cano Fabiola E
Department of Anatomy & Neurobiology
Eye Proteins/*genetics
Frara Nagat A
Inbred DBA
Lababidi Suzanne L
Male
Membrane Glycoproteins/*genetics
Mice
Moussa Fouad M
Mutation
NEOMED College of Medicine
Newborn
Novak Kimberly M
Osteoblasts/cytology/*physiology
Osteocalcin/*genetics
Osteogenesis/*genetics
Phenotype
Razmpour Roshanak
Receptors
Safadi Fayez F
Sanyurah Afif S
Sondag Gregory R
The American journal of pathology
Transforming Growth Factor beta/metabolism