2004
DOI: 10.1016/s0002-9440(10)63172-0
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Impaired Calcification Around Matrix Vesicles of Growth Plate and Bone in Alkaline Phosphatase-Deficient Mice

Abstract: The presence of skeletal hypomineralization was confirmed in mice lacking the gene for bone alkaline phosphatase, ie, the tissue-non-specific isozyme of alkaline phosphatase (TNAP). In this study, a detailed characterization of the ultrastructural localization, the relative amount and ultrastructural morphology of bone mineral was carried out in tibial growth plates and in subjacent metaphyseal bone of 10-day-old TNAP knockout mice. Alizarin red staining, microcomputerized tomography (micro CT), and FTIR imagi… Show more

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Cited by 329 publications
(245 citation statements)
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References 26 publications
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“…Several human and mouse diseases with excessive or insufficient bone formation have been related to defects in, respectively, the phosphodiesterases (such as nucleotide pyrophosphatase/phosphodiesterase 1), which produce PPi (11,12), and the phosphatases (such as tissue-nonspecific alkaline phosphatase [TNAP]), which degrade PPi (13)(14)(15). The homozygous ank (progressive ankylosis) mouse has a loss-of-function nonsense mutation in the ank gene that codes for a regulator of PPi export, and these mice develop a condition characterized by pathologic calcium apatite crystal deposition in the synovial and subsynovial spaces, followed by chondro-osteophyte formation and eventual bony ankylosis of the affected joints (16).…”
Section: Conclusion Our Results Indicate That the Tnap Haplotype Rs3mentioning
confidence: 99%
“…Several human and mouse diseases with excessive or insufficient bone formation have been related to defects in, respectively, the phosphodiesterases (such as nucleotide pyrophosphatase/phosphodiesterase 1), which produce PPi (11,12), and the phosphatases (such as tissue-nonspecific alkaline phosphatase [TNAP]), which degrade PPi (13)(14)(15). The homozygous ank (progressive ankylosis) mouse has a loss-of-function nonsense mutation in the ank gene that codes for a regulator of PPi export, and these mice develop a condition characterized by pathologic calcium apatite crystal deposition in the synovial and subsynovial spaces, followed by chondro-osteophyte formation and eventual bony ankylosis of the affected joints (16).…”
Section: Conclusion Our Results Indicate That the Tnap Haplotype Rs3mentioning
confidence: 99%
“…ALP activity has been shown inside matrix vesicles shed from chondrocytes and most likely works to increase the availabil- ity of inorganic phosphate (P i ) needed for hydroxyapatite crystal growth. 30 Increases in ALP activity is a marker of the transition to an osteogenic phenotype by smooth muscle cells in vitro. ALP activity is increased after exposure of smooth muscle cells to inflammatory factors.…”
Section: Discussionmentioning
confidence: 99%
“…Accordingly, mutations in the TNAP gene that cause impairment or loss of functional activity lead to hypophosphatasia in humans [486,487]. Similarly, TNAP knockout mice (Akp2−/−) accumulate extracellular PP i , reveal hypomineralization [488][489][490][491], and can serve as a model for the infantile form of hypophosphatasia [492]. The defect can be eliminated by subcutaneous injections of soluble TNAP targeted to mineralizing tissue [493,494] or by lentiviral application of a bone-targeted form of TNAP [495].…”
Section: Substrates and Catalytic Propertiesmentioning
confidence: 99%