Rapidly Forming Apatitic Mineral in an Osteoblastic Cell Line (UMR 106—01 BSP)

Stanford, Clark M.; Jacobson, Petra; Eanes, E. D.; Lembke, Lois A.; Midura, Ronald J.

doi:10.1074/jbc.270.16.9420

Cited by 406 publications

(318 citation statements)

References 42 publications

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“…The stained cells were imaged using a digital camera (Nikon, Tokyo, Japan). The amount of Alizarin Red S dye released from the extracellular matrix after incubation in 100 mM aqueous cetylpyridinium chloride solution was quantified by spectrophotometry at 550 nm [16].…”

Section: Identification Of Calcificationmentioning

confidence: 99%

CD34-negative mesenchymal stem-like cells may act as the cellular origin of human aortic valve calcification

Nomura

Seya

et al. 2013

Biochemical and Biophysical Research Communications

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Although various osteogenic inducers contribute to the calcification of human aortic valve interstitial cells, the cellular origin of calcification remains unclear. We immunohistochemically investigated the cellular origin of valve calcification using enzymatically isolated cells from both calcified and non-calcified human aortic valve specimens. CD73-, 90-, and 105-positive and CD45-negative mesenchymal stem-like cells (MSLCs) were isolated from both types of valve specimens using fluorescence-activated cell sorting. MSLCs were further sorted into CD34-negative and -positive cells. Compared with CD34-positive cells, CD34-negative MSLCs were significantly more sensitive to high inorganic phosphate (3.2 mM), calcifying easily in response. Furthermore, immunohistochemical staining showed that significantly higher numbers (～7-9-fold) of CD34-negative compared with CD34-positive MSLCs were localized in calcified aortic valve specimens obtained from calcified aortic stenosis patients. These results suggest that CD34-negative MSLCs are responsible for calcification of the aortic valve.

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Section: Identification Of Calcificationmentioning

confidence: 99%

CD34-negative mesenchymal stem-like cells may act as the cellular origin of human aortic valve calcification

Nomura

Seya

et al. 2013

Biochemical and Biophysical Research Communications

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“…21,22,32 Osteogenic supplemented medium contains ascorbic acid and ß-glycerophosphate to stimulate greater collagen production and cross-linking. 33 To enhance osteogenesis further, the synthetic glucocorticoid dexamethasone is often added. Dexamethasone, however, was omitted as it was proven in rat bone marrow stromal cells that dexamethasone per se acts at multiple points in the differentiation process to stimulate osteoblastic maturation.…”

Section: Osteogenic Supplemented Mediamentioning

confidence: 99%

Effects of arachidonic acid and docosahexaenoic acid on differentiation and mineralization of MC3T3‐E1 osteoblast‐like cells

Coetzee

Haag

Kruger

2008

Cell Biochemistry & Function

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Osteoblasts in culture can differentiate into mature mineralizing osteoblasts when stimulated with osteogenic agents. Clinical trials and in vivo animal studies suggest that specific polyunsaturated fatty acids (PUFAs) may benefit bone health. The aim of this study was to investigate whether arachidonic acid (AA) and docosahexaenoic acid (DHA) affect osteogenesis in osteoblasts and the transdifferentiation into adipocytes. Results from this study show that long-term exposure to AA inhibited alkaline phosphatase (ALP) activity in these cells, which might be prostaglandin E 2 (PGE 2 )-mediated. DHA exposure also inhibited ALP activity which was evident after both short-and long-term exposures. The mechanism whereby DHA inhibits ALP activity is not clear and needs to be investigated. Although long-term exposure to PUFAs inhibited ALP activity, the mineralizing properties of these cells were not compromised. Furthermore, PUFA exposure did not induce adipocyte-like features in these cells as evidenced by the lack of cytoplasmic triacylglycerol accummulation. More research is required to elucidate the cellular mechanisms of action of PUFAs on bone.

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“…Cells were rinsed with distilled H 2 O and stained in 1% alizarin red S (GFS chemicals) for 30 -60 min at room temperature. Mineralization was visualized following several rinses with distilled H 2 O. Quantification of mineralization was performed by dissolving stained mineralized cultures in 10% cetylpyridinium chloride, followed by reading absorbance at 540 nM (34).…”

Section: Methodsmentioning

confidence: 99%

Identification of the GATA Factor TRPS1 as a Repressor of the Osteocalcin Promoter

Piscopo

Johansen

Derynck

2009

Journal of Biological Chemistry

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A proteomic analysis of proteins bound to the osteocalcin OSE2 sequence of the mouse osteocalcin promoter identified TRPS1 as a regulator of osteocalcin transcription. Mutations in the TRPS1 gene are responsible for human tricho-rhino-phalangeal syndrome, which is characterized by skeletal and craniofacial abnormalities. TRPS1 has been shown to bind regulatory promoter sequences containing GATA consensus binding sites and to repress transcription of genes involved in chondrocyte differentiation. Here we show that TRPS1 can directly bind the osteocalcin promoter in the presence or absence of Runx2. TRPS1 binds through a GATA binding sequence in the proximal promoter of the osteocalcin gene. The GATA binding site is conserved in mice, humans, and rats, although its location and orientation are not. Mutation of the mouse or human GATA binding sequence abrogates binding of TRPS1 to the osteocalcin promoter. We show that TRPS1 is expressed in osteosarcoma cells and upon induction of osteoblast differentiation in primary mouse bone marrow stromal cells and that TRPS1 regulates the expression of osteocalcin in both cell types. The expression of TRPS1 modulates mineralized bone matrix formation in differentiating osteoblast cells. These data suggest a role for TRPS1 in osteoblast differentiation, in addition to its previously described role in chondrogenesis.Runx2, previously described as CBFA1, OSF2, AML3, or PEPB2␣A, is a runt homology domain transcription factor and plays a key role in driving osteoblast differentiation. Runx2 expression, which occurs in differentiating and mature osteoblasts, is essential for bone formation, as illustrated by the phenotype of Runx2-deficient mice, which lack osteoblasts and have skeletons that are primarily composed of immature chondrocytes (1-3). Haploinsufficiency for RUNX2 in humans results in cleidocranial dysplasia, a syndrome that is characterized by delayed endochondral and intramembranous ossification (4). Runx2 transactivates genes involved in the deposition of bone matrix, e.g. those encoding osteocalcin, collagen IA1, osteopontin, and matrix metalloproteinase 13 (MMP13), and regulation of osteoclastogenesis, e.g. the genes encoding RankL and osteoprotegerin (reviewed in Ref. 5). Although Runx2 is expressed in cells of the osteoblast lineage throughout skeletal development, its levels increase only 1.5-2-fold as preosteoblasts differentiate into mature osteoblasts. Furthermore, the amount of Runx2 bound to target promoters, as measured by chromatin immunoprecipitation, is relatively unchanged throughout differentiation (6), yet the targets it regulates have distinct patterns of expression. These observations suggest that the regulation of Runx2 activity, either by post-translational modification or by the binding of co-regulators, plays a substantial role in defining the Runx2-mediated activation of target genes. Various proteins have been shown to interact with Runx2 and modulate its activity, including Smad3, CREB 2 -binding protein (CBP) HES1, Groucho/TLE, and histone d...

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Rapidly Forming Apatitic Mineral in an Osteoblastic Cell Line (UMR 106—01 BSP)

Cited by 406 publications

References 42 publications

CD34-negative mesenchymal stem-like cells may act as the cellular origin of human aortic valve calcification

CD34-negative mesenchymal stem-like cells may act as the cellular origin of human aortic valve calcification

Effects of arachidonic acid and docosahexaenoic acid on differentiation and mineralization of MC3T3‐E1 osteoblast‐like cells

Identification of the GATA Factor TRPS1 as a Repressor of the Osteocalcin Promoter

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