Osteoblastic Cell Response and Bone Formation of Phosphate Ion Coated on Plasma Polymerized Ti Surface

2013 ◽  
Vol 13 (1) ◽  
pp. 698-701
Author(s):  
Seong-Won Yang ◽  
Kang Lee ◽  
Byung-Hoon Kim
Keyword(s):  
Bone Formation ◽  
Cell Response ◽  
Osteoblastic Cell ◽  
Phosphate Ion

scholarly journals Suppression of Wnt Signaling by Dkk1 Attenuates PTH-Mediated Stromal Cell Response and New Bone Formation

2010 ◽  
Vol 11 (2) ◽  
pp. 161-171 ◽  
Author(s):  
Jun Guo ◽  
Minlin Liu ◽  
Dehong Yang ◽  
Mary L. Bouxsein ◽  
Hiroaki Saito ◽  
...  
Keyword(s):  
Bone Formation ◽  
Wnt Signaling ◽  
Cell Response ◽  
Stromal Cell ◽  
New Bone Formation

scholarly journals Surface characteristics and osteoblastic cell response of alkali-and heat-treated titanium-8tantalum-3niobium alloy

2012 ◽  
Vol 42 (6) ◽  
pp. 248 ◽  
Author(s):  
Bo-Ah Lee ◽  
Choong-Hee Kang ◽  
Mong-Sook Vang ◽  
Young-Suk Jung ◽  
Xing Hui Piao ◽  
...  
Keyword(s):  
Cell Response ◽  
Surface Characteristics ◽  
Osteoblastic Cell ◽  
Heat Treated

scholarly journals Maternal obesity impairs skeletal development in adult offspring

2018 ◽  
Vol 239 (1) ◽  
pp. 33-47 ◽  
Author(s):  
Jin-Ran Chen ◽  
Oxana P Lazarenko ◽  
Haijun Zhao ◽  
Alexander W Alund ◽  
Kartik Shankar
Keyword(s):  
Bone Formation ◽  
Maternal Obesity ◽  
Skeletal Development ◽  
Prenatal Development ◽  
Cell Senescence ◽  
Inflammatory Factors ◽  
Osteoblastic Cell ◽  
Human Umbilical Cord ◽  
Adult Offspring ◽  
Embryonic Mouse

Intrauterine or early postnatal high-fat diet (HFD) has substantial influences on adult offspring health; however, studies of HFD-induced maternal obesity on regulation of adult offspring bone formation are sparse. Here, we investigated the effects of HFD-induced maternal obesity on both fetal and adult offspring skeletal development. We found that HFD-induced maternal obesity significantly decreased fetal skeletal development, but enhanced fetal osteoblastic cell senescence signaling and significantly increased the expression of inflammatory factors of the senescence-associated secretory phenotype (SASP) in osteo-progenitors. It was found that p300/CBP activation led to H3K27 acetylation to increase the expression of senescence-related genes and PPARγ in embryonic mouse osteogenic calvarial cells from HFD obese dams. These results were recapitulated in human umbilical cord mesenchymal stem cells (UC MSCs) isolated from offspring of pregnant obese and lean mothers following delivery. Regardless of postnatal HFD challenge, adult offspring from HFD obese dams showed significantly suppressed bone formation. Such early involution of bone formation of adult offspring from HFD obese dams may at least in part due to histone acetylation, i.e., epigenetic regulation of genes involved in cell senescence signaling in pre-osteoblasts from prenatal development. These findings indicate fetal pre-osteoblastic cell senescence signaling is epigenetically regulated by maternal obesity to repress bone formation in adult offspring in rodents and suggest that at least some of these effects may also manifest in humans.

scholarly journals The Effects of Dickkopf-4 on the Proliferation, Differentiation, and Apoptosis of Osteoblasts

Endocrinology ◽  
2013 ◽  
Vol 154 (12) ◽  
pp. 4618-4626 ◽  
Author(s):  
Shiro Hiramitsu ◽  
Masakazu Terauchi ◽  
Toshiro Kubota
Keyword(s):  
Alkaline Phosphatase ◽  
Bone Formation ◽  
Target Genes ◽  
Osteoblastic Cell ◽  
Osteoblastic Cell Line ◽  
Alkaline Phosphatase Assay ◽  
Proliferation And Differentiation ◽  
Phosphatase Assay ◽  
Rna Knockdown ◽  
Interfering Rna

The Dickkopf family of proteins is comprised of four members (Dkk1, Dkk2, Dkk3, Dkk4) that are known to modulate Wnt/β-catenin signaling, which is activated during bone formation. Although the effects of Dkk1 on Wnt/β-catenin signaling have been well studied, little is known about the effects of Dkk4. Therefore, to evaluate the role of Dkk4 in osteoblastogenesis, we used the mouse osteoblastic cell line MC3T3-E1, in which Dkk4 expression was suppressed by small interfering RNA knockdown. Our results showed that the suppression of Dkk4 expression promoted osteoblast proliferation and differentiation and suppressed apoptosis. In colony-forming unit alkaline phosphatase assay, Dkk4 knockdown cells possessed markedly higher alkaline phosphatase activity compared with Dkk1 knockdown cells. Reduced Dkk4 expression also led to the up-regulation of β-catenin levels, β-catenin/T cell factor activity, and Wnt-target genes. In contrast, overexpression of Dkk4 in MC3T3-E1 cells led to inhibition of osteoblast differentiation. Our findings reveal that Dkk4 functions as an inhibitor of osteoblastogenesis through Wnt/β-catenin signaling, providing new insights into the relationship between Wnt/β-catenin signaling and Dkk4 in bone formation.

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