Studies on matrix vesicles isolated from chick epiphyseal cartilage Association of pyrophosphatase and ATPase activities with alkaline phosphatase

Majeska, Robert J.; Wuthier, Roy E.

doi:10.1016/0005-2744(75)90151-5

Cited by 260 publications

(124 citation statements)

References 24 publications

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“…Alkaline phosphatase is an enzyme marker of osteoblasts, and the enzyme participates in bone mineralization (31). ·1 (I) collagen is a matrix protein that is related to bone formation and mineralization in osteoblast lineage cells (32).…”

Section: Discussionmentioning

confidence: 99%

Genistein and zinc synergistically enhance gene expression and mineralization in osteoblastic MC3T3-E1 cells

Uchiyama

Yamaguchi²

2007

Int J Mol Med

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Section: Discussionmentioning

confidence: 99%

Genistein and zinc synergistically enhance gene expression and mineralization in osteoblastic MC3T3-E1 cells

Uchiyama

Yamaguchi²

2007

Int J Mol Med

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“…4B). Discussion ß-cryptoxanthin has been shown to have a stimulatory effect on osteoblastic bone formation in vitro (6,7) and in vivo (10)(11)(12) by stimulating osteoblastic cell proliferation and differentiation and by regulating osteoblastic gene expression, including Runx2 a master regulator of osteoblast differentiation (26,28), the matrix protein of ·1 (I) collagen (6,29), and alkaline phosphatase which participates in the mineralization process (6,30). The molecular mechanism by which ß-cryptoxanthin promotes osteoblast differentiation is, however, poorly defined.…”

Section: ß-Cryptoxanthin Stimulates Osteoblastic Mineralizationmentioning

confidence: 99%

The bone anabolic carotenoid β-cryptoxanthin enhances transforming growth factor-β1-induced SMAD activation in MC3T3 preosteoblasts

Yamaguchi¹

2009

Int J Mol Med

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Abstract. The xanthophyll ß-cryptoxanthin is a member of the carotenoid family of plant-derived pigments endowed with anti-osteoporotic properties in vivo. ß-cryptoxanthin was demonstrated to stimulate osteoblastic bone formation and simultaneously repress osteoclastic bone resorption in vitro. However, the mechanisms of action remain to be elucidated. The SMAD signal transduction pathway is established to play a critical role in osteoblast lineage commitment and differentiation. In this study we used transient transfection assays of a SMAD luciferase reporter to investigate whether ß-cryptoxanthin regulates SMAD activation in MC3T3 preosteoblastic cells. ß-cryptoxanthin did not stimulate basal SMAD activity but amplified transforming growth factor (TGF)-ß1-induced SMAD activation. Interestingly, ß-cryptoxanthin did not affect bone morphogenetic protein-2 (BMP-2)-induced SMAD activation in osteoblastic cells, suggesting specificity of action on the TGF-ß1 pathway. This study suggests that the carotenoid ß-cryptoxanthin may promote osteoblast differentiation and activity by amplifying TGF-ß1-induced lineage commitment of osteoblast precursors.

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“…The severity and expressivity of hypophosphatasia depends on the nature of the TNAP mutation (6). TNAP is present in MVs (7), and it has been proposed that the inorganic phosphate (P i )-generating activity of TNAP is required to generate the P i needed for hydroxyapatite crystallization (8)(9)(10). However, the ability of TNAP to hydrolyze PP i also has been hypothesized to be important to promote osteoblastic mineralization (11,12), because PP i suppresses the formation and growth of hydroxyapatite crystals (13).…”

mentioning

confidence: 99%

Tissue-nonspecific alkaline phosphatase and plasma cell membrane glycoprotein-1 are central antagonistic regulators of bone mineralization

Hessle

Johnson

Anderson

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

775

629

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I n the process of bone formation, osteoblasts mineralize the matrix by promoting the seeding of basic calcium phosphate crystals of hydroxyapatite in the sheltered interior of shed membrane-limited matrix vesicles (MVs) and by propagating hydroxyapatite mineral onto the collagenous extracellular matrix (osteoid; refs. 1 and 2). Tissue-nonspecific alkaline phosphatase (TNAP), an isozyme of a family of four homologous human alkaline phosphatase genes (3), plays a role in bone matrix mineralization. Deactivating mutations in the TNAP gene causes the inborn error of metabolism known as hypophosphatasia (4), characterized by poorly mineralized cartilage (rickets) and bones (osteomalacia), spontaneous bone fractures, and elevated extracellular inorganic pyrophosphate (PP i ) concentrations (5). The severity and expressivity of hypophosphatasia depends on the nature of the TNAP mutation (6). TNAP is present in MVs (7), and it has been proposed that the inorganic phosphate (P i )-generating activity of TNAP is required to generate the P i needed for hydroxyapatite crystallization (8-10). However, the ability of TNAP to hydrolyze PP i also has been hypothesized to be important to promote osteoblastic mineralization (11, 12), because PP i suppresses the formation and growth of hydroxyapatite crystals (13). In fact, heritable extracellular PP i deficiencies are models of ectopic calcification such as ankylosing spinal hyperostosis and pathologic soft-tissue ossification (14-16). PP i is produced by the nucleoside triphosphate pyrophosphohydrolase (NTPPPH) activity of a family of isozymes that include PC-1, B10͞PDNP3, and autotaxin (17-19). However, PC-1 seems to be the only NTPPPH present in MVs (20). TNAP knockout (KO) mice (21-23) recapitulate the heritable metabolic disease hypophosphatasia (5), whereas PC-1-null mice display hypermineralization abnormalities similar to cartilage calcification in osteoarthritis (14) and ossification of the posterior longitudinal ligament of the spine (15).We previously identified PC-1 as the likely NTPPPH isozyme to act on the same pathway with TNAP as antagonistic regulators of extracellular PP i concentrations (20). In this paper, we have tested the hypothesis that bone abnormalities caused by the lack of TNAP could be counterbalanced by the removal of PC-1 and vice versa. We show that bone mineralization in double-KO mice lacking both TNAP and PC-1 is essentially normal, providing evidence that TNAP and PC-1 are key regulators of bone mineralization by determining the normal steady-state levels of PP i . Our work suggests that TNAP and PC-1 may be useful therapeutic targets for the treatment of bone mineralization abnormalities. Materials and MethodsAkp2 and Enpp1 KO Mice. The generation and characterization of the Akp2 KO mice has been reported (22,23). These Akp2 KO mice were hybrids of C57BL͞6 ϫ 129͞J mouse strains. The generation of the Enpp1 KO mice has been reported briefly (24). These Enpp1 KO mice were hybrids of C57BL͞6 ϫ 129͞SvTerJ mouse strains. Akp2͞Enpp1 double-heterozy...

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Studies on matrix vesicles isolated from chick epiphyseal cartilage Association of pyrophosphatase and ATPase activities with alkaline phosphatase

Cited by 260 publications

References 24 publications

Genistein and zinc synergistically enhance gene expression and mineralization in osteoblastic MC3T3-E1 cells

Genistein and zinc synergistically enhance gene expression and mineralization in osteoblastic MC3T3-E1 cells

The bone anabolic carotenoid β-cryptoxanthin enhances transforming growth factor-β1-induced SMAD activation in MC3T3 preosteoblasts

Tissue-nonspecific alkaline phosphatase and plasma cell membrane glycoprotein-1 are central antagonistic regulators of bone mineralization

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