Inhibition of hydroxyapatite-crystal growth by bone-specific and other calcium-binding proteins

Romberg, Robert W.; Werness, P. G.; Riggs, B. Lawrence; Mann, Kenneth G.

doi:10.1021/bi00353a035

Cited by 298 publications

(181 citation statements)

References 38 publications

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“…Damsky and colleagues have demonstrated that osteoblast/fibronectin interactions supply a necessary regulatory signal essential for osteogenic gene expression, with fibronectin possibly playing a role in the recruitment of osteoblast precursor cells (Globus et al, 1995;Moursi et al, 1996;Globus et al, 1998). Finally, osteonectin/SPARC is one of the most abundant noncollagenous proteins found in bone, and it binds strongly to hydroxyapatite (Romberg et al, 1985;Romberg et al, 1986) and collagen I (Kelm, Jr. et al, 1991). Null mutations in osteonectin result in a reduced number of osteoblasts and poor bone maturation, as well as a reduction in matrix production and assembly (Boskey et al, 2003;Delany et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Laminin-5 activates extracellular matrix production and osteogenic gene focusing in human mesenchymal stem cells

et al. 2007

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We recently reported that laminin-5, expressed by human mesenchymal stem cells (hMSC), stimulates osteogenic gene expression in these cells in the absence of any other osteogenic stimulus. Here we employ two dimensional liquid chromatography and tandem mass spectrometry, along with the Database for Annotation, Visualization and Integrated Discovery (DAVID), to obtain a more comprehensive profile of the protein (and hence gene) expression changes occurring during laminin-5-induced osteogenesis of hMSC. Specifically, we compare the protein expression profiles of undifferentiated hMSC, hMSC cultured on laminin-5 (Ln-5 hMSC), and fully differentiated human osteoblasts (hOST) with profiles from hMSC treated with well-established osteogenic stimuli (collagen I, vitronectin, or dexamethazone). We find a marked reduction in the number of proteins (e.g., those involved with calcium signaling and cellular metabolism) expressed in Ln-5 hMSC compared to hMSC, consistent with our previous finding that hOST express far fewer proteins than do their hMSC progenitors, a pattern we call "osteogenic gene focusing." This focused set, which resembles an intermediate stage between hMSC and mature hOST, mirrors the expression profiles of hMSC exposed to established osteogenic stimuli and includes osteogenic extracellular matrix proteins (collagen, vitronectin) and their integrin receptors, calcium signaling proteins, and enzymes involved in lipid metabolism. These results provide direct evidence that laminin-5 alone stimulates global changes in gene/protein expression in hMSC that lead to commitment of these cells to the osteogenic phenotype, and that this commitment correlates with extracellular matrix production.

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Section: Discussionmentioning

confidence: 99%

Laminin-5 activates extracellular matrix production and osteogenic gene focusing in human mesenchymal stem cells

et al. 2007

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“…Additional work has indicated that osteonectin, and to a lesser extent osteocalcin, could inhibit hydroxyapatite crystal formation. 54 This role seems to prevent excessive mineralization in bone. Osteonectin and osteocalcin are detectable in normal plasma and serum 40,55 and together with osteopontin are also present in human platelets.…”

Section: Role Of Bone-related Noncollagenous Proteins In Atherosclermentioning

confidence: 99%

Noncollagenous Bone Matrix Proteins, Calcification, and Thrombosis in Carotid Artery Atherosclerosis

Bini

Mann

Kudryk

et al. 1999

ATVB

Self Cite

141

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Abstract-Advanced atherosclerosis is often associated with dystrophic calcification, which may contribute to plaque rupture and thrombosis. In this work, the localization and association of the noncollagenous bone matrix proteins osteonectin, osteopontin, and osteocalcin with calcification, lipoproteins, thrombus/hemorrhage (T/H), and matrix metalloproteinases (MMPs) in human carotid arteries from endarterectomy samples have been determined. According to the recent American Heart Association classification, 6 of the advanced lesions studied were type V (fibroatheroma) and 16 type VI (complicated 4 and ex vivo 5 detection of calcium deposits in coronary arteries, have shown that calcification is correlated with atherosclerotic plaque burden and that noninvasive detection of calcification may have predictive value in the development of subsequent coronary events. 5 The molecular determinants regulating extracellular matrix calcification have yet to be identified. Recent studies have shown that noncollagenous bone matrix proteins such as osteonectin, osteocalcin, and osteopontin are also found in atherosclerotic vessels and may regulate dystrophic calcification. For example, osteonectin (SPARC) has been identified in vessel wall cells 6 and platelets 7 and participates in the regulation of bone mineralization, 8 cell migration/proliferation, 9 and remodeling of extracellular matrix. 10 -12 Recently, it has been shown that osteonectin binds to plasminogen, 13 increases its activation and binding to collagen, 13 and induces the expression of type 1 plasminogen activator inhibitor in endothelial cells (ECs). 14 That suggests a role for osteonectin in both the degradation of extracellular matrix and the regulation of fibrinolysis. Moreover, osteonectin upregulates the expression of matrix metalloproteinases (MMPs) in cultured fibroblasts. 15 Previous studies have implicated MMPs in destabilization and rupture of atherosclerotic plaques, 16 -19 and we recently showed that both fibrinogen and cross-linked fibrin, proteins known to be associated with both early and complicated plaques, can be degraded by MMP-2,

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“…The postulated roles of matrix proteins are diverse: a nucleator by providing certain stereochemical arrangement of charged groups, which is sufficient to lower the activation energy barrier for nucleation of a crystal phase (Glimcher, 1989;Gorski, 1992); or an inhibitor by blocking the growth sites through specific adsorption (Moreno et al, 1979;Termine et al, 1980;Romberg et al, 1986) or by providing spacial constraints as exemplified by the lateral growth of apatitic mineral in calcified turkey tendon (Heywood et al, 1990). Casein phosphoproteins in milk, as cited above, act as a stabilizer of amorphous calcium phosphate in nanometer-sized clusters (Holt et al, 1996).…”

Section: Interaction Between Macromolecules and Calcium Phosphatesmentioning

confidence: 99%

The Effect of Fluoride On Apatite Structure and Growth

Aoba

1997

Critical Reviews in Oral Biology & Medicine

189

120

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Fluoride participates in many aspects of calcium phosphate formation in vivo and has enormous effects on the process and on the nature and properties of formed mineral. The most well-documented effect of fluoride is that this ion substitutes for a column hydroxyl in the apatite structure, giving rise to a reduction of crystal volume and a concomitant increase in structural stability. In the process of enamel mineralization during amelogenesis (a unique model for the cell-mediated formation of well-crystallized carbonatoapatite), free fluoride ions in the fluid phase are supposed to accelerate the hydrolysis of acidic precursor(s) and increase the driving force for the growth of apatitic mineral. Once fluoride is incorporated into the enamel mineral, the ion likely affects the subsequent mineralization process by reducing the solubility of the mineral and thereby modulating the ionic composition in the fluid surrounding the mineral, and enhancing the matrix protein-mineral interaction. But excess fluoride leads to anomalous enamel formation by retarding tissue maturation. It is worth noting that enameloid/enamel minerals found in vertebrate teeth have a wide range of CO3 and fluoride substitutions. In the evolutionary process from elasmobranch through teleost enameloid to mammalian enamel, the biosystems appear to develop regulatory functions for limiting the fluoridation of the formed mineral, but this development is accompanied by an increase of carbonate substitution or defects in the mineral. In research on the cariostatic effect of fluoride, considerable emphasis is placed on the roles of free fluoride ions (i.e., preventing the dissolution and accelerating the kinetics of remineralization) in the oral fluid bathing tooth mineral. Fluoride also has been used for the treatment of osteoporosis, but much still remains to be learned about maximizing the benefit and minimizing the risk of fluoride when used as a public health measure.

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Inhibition of hydroxyapatite-crystal growth by bone-specific and other calcium-binding proteins

Cited by 298 publications

References 38 publications

Laminin-5 activates extracellular matrix production and osteogenic gene focusing in human mesenchymal stem cells

Laminin-5 activates extracellular matrix production and osteogenic gene focusing in human mesenchymal stem cells

Noncollagenous Bone Matrix Proteins, Calcification, and Thrombosis in Carotid Artery Atherosclerosis

The Effect of Fluoride On Apatite Structure and Growth

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