Osteoadherin is Upregulated by Mature Osteoblasts and Enhances Their In Vitro Differentiation and Mineralization

Rehn, Anders; Černý, Rudolf; Sugars, Rachael V.; Kaukua, Nina; Wendel, Mikael

doi:10.1007/s00223-008-9138-1

Cited by 50 publications

(32 citation statements)

References 215 publications

(182 reference statements)

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“…Increasing TNAP activity is a prerequisite for increasing phosphate amounts at the site of mineralization and lead in consequence to increasing calcium phosphate deposition. Osteoadherin (¼osteomodulin, OSAD) is an extracellular matrix keratan sulfate-containing proteoglycan which is involved in a controlling mineralization process in bones and teeth [45]. Other typical osteogenic markers as collagen typ 1, osterix, and osteocalcin are suppressed by dex [41,43].…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin E2 impairs osteogenic and facilitates adipogenic differentiation of human bone marrow stromal cells

Noack¹,

Hempel²,

Preissler

et al. 2015

Prostaglandins, Leukotrienes and Essential Fatty Acids

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Section: Discussionmentioning

confidence: 99%

Prostaglandin E2 impairs osteogenic and facilitates adipogenic differentiation of human bone marrow stromal cells

Noack¹,

Hempel²,

Preissler

et al. 2015

Prostaglandins, Leukotrienes and Essential Fatty Acids

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“…2C) which belong to the small leucine rich repeat family (SLRP) show increased expression in osteoblasts during differentiation [21,22]. Recent published studies show 1) that when 2T3 cells (preosteoblast cells) become confluent in culture, they increase expression of Osterix , DLX5, BMP2 and Osteomodulin [23] and 2) over expression of Osteomodulin in vitro leads to increased osteoblast differentiation [24]. We also observed that Runx2 the major osteoblast transcriptional factor and its target gene Osteocalcin are upregulated.…”

Section: Discussionmentioning

confidence: 99%

N-cadherin adherens junctions mediate osteogenesis through PI3K signaling

Guntur

Rosen

Naski

2012

Bone

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During endochondral ossification, the cartilage is surrounded by a layer of cells that constitute the perichondrium. Communication between osteoblasts in the perichondrium via N-cadherin adherens junctions is essential for endochondral bone growth. We observed that adherens junction molecule N-cadherin and its interacting partners p120, β-catenin and PTEN are expressed by cells present in the perichondrium. To study if N-cadherin mediated adherens junctions play a role in mediating signal transduction events during bone development, we utilized MC3T3E1 preosteoblasts plated at sub confluent (low) and confluent (high) densities to mimic adherens junction formation. When MC3T3E1 cells were plated at high density we observed an increase in phosphorylation of AKTSer473 and its downstream target GSK3Ser9, which coincided with an increase in Osterix, Osteomodulin and Osteoglycin gene expression. Using immunofluorescence, we identified N-cadherin, p120 and β-catenin localized at the membrane of MC3T3E1 cells. Treatment of confluent MC3T3E1cells with an N-cadherin junction inhibitor-EGTA and a PI3K inhibitor LY294002 resulted in reduction of phosphorylation levels of AKT and GSK3 and expression of Osterix, Osteomodulin and Osteoglycin. Furthermore, utilizing an N-cadherin blocking antibody resulted in reduced AKT signaling and Osterix gene expression, suggesting that osteoblast junction formation is linked to activation of PI3K signaling, which leads to osteoblast differentiation. To further explore the strength of this linkage, we utilized a conditional knockout approach using Dermo1cre to delete β-catenin and PTEN, two important proteins known to be essential for adherens junctions and PI3K signaling, respectively. In the absence of β-catenin, we observed a decrease in adherens junctions and AKT signaling in the perichondrium. PTEN deletion, on the other hand, increased the number of cells expressing N-cadherin in the perichondrium. These observations show that N-cadherin mediated junctions between osteoblasts are needed for osteoblast gene transcription.

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“…expressions were induced 18) . Interestingly, OMD gene overexpression in MC3T3-E1 cells resulted in an increase of osteoblastic differentiation features, such as increased alkaline phosphatase activity and increased in vitro mineralization 19) .…”

Section: Discussionmentioning

confidence: 99%

Hydrogen Peroxide Reduced Osteomodulin Gene Expression in MC3T3-E1

Kamikawa

Abiko

2009

J. Hard Tissue Biology.

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: Bone formation steadily declines with age resulting in significant loss of bone mass, and reactive oxygen species (ROS) are thought to be a major contributor to the aging process. H2O2 treatment significantly reduced bone nodule formation rate in pre-osteoblastic cell, MC3T3E1. In this study, to identify which genes have an altered transcription level associated with bone loss by ageing, MC3T3-E1 cells were treated with H2O2, and monitored gene expression change using the Affymetrix GeneChip TM system (Mouse; 34,000 genes). H2O2 altered many gene expressions including reduction of osteomodulin (OMD) mRNA level. The reduction of OMD gene expression by H2O2 was successfully confirmed by reversed transcription polymerase chain reaction (RT-PCR) and real-time PCR. Since OMD was found in bone tissues and play an important role in biomineralization, the reduction of OMD gene expression by H2O2 may be involved in the decline of bone formation in the ageing process.

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Osteoadherin is Upregulated by Mature Osteoblasts and Enhances Their In Vitro Differentiation and Mineralization

Cited by 50 publications

References 215 publications

Prostaglandin E2 impairs osteogenic and facilitates adipogenic differentiation of human bone marrow stromal cells

Prostaglandin E2 impairs osteogenic and facilitates adipogenic differentiation of human bone marrow stromal cells

N-cadherin adherens junctions mediate osteogenesis through PI3K signaling

Hydrogen Peroxide Reduced Osteomodulin Gene Expression in MC3T3-E1

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