The roles of annexins and alkaline phosphatase in mineralization process.

Balcerzak, Marcin; Hamade, Eva; Zhang, Le; Pikula, Sławomir; Azzar, Gérard; Radisson, J.; Bandorowicz‐Pikuła, Joanna; Buchet, René

doi:10.18388/abp.2003_3629

Cited by 182 publications

(86 citation statements)

References 162 publications

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“…Osteoblast maturation can be divided into proliferation, differentiation and matrix mineralization. 15,16 IGF-1 treatment enhances the early phase of osteoblast proliferation, whereas it inhibited the gene expression of osteocalcin, a marker for differentiating osteoblasts. We have shown that IGF-1 regulates osteoblast proliferation via Akt and MAP kinase pathway.…”

Section: Discussionmentioning

confidence: 99%

Effects of insulin and insulin‐like growth factor 1 on osteoblast proliferation and differentiation: differential signalling via Akt and ERK

Zhang

Shen

Wan

et al. 2012

Cell Biochemistry & Function

111

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Insulin and insulin-like growth factor 1 (IGF-1) are evolutionarily conserved hormonal signalling molecules, which influence a wide array of physiological functions including metabolism, growth and development. Using genetic mouse studies, both insulin and IGF-1 have been shown to be anabolic agents in osteoblasts and bone development primarily through the activation of Akt and ERK signalling pathways. In this study, we examined the temporal signalling actions of insulin and IGF-1 on primary calvarial osteoblast growth and differentiation. First, we observed that the IGF-1 receptor expression decreases whereas insulin receptor expression increases during osteoblast differentiation. Subsequently, we show that although both insulin and IGF-1 promote osteoblast differentiation and mineralization in vitro, IGF-1, but not insulin, can induce osteoblast proliferation. The IGF-1-induced osteoblast proliferation was mediated via both MAPK and Akt pathways because the IGF-1-mediated cell proliferation was blocked by U0126, an MEK/MAPK inhibitor, or LY294002, a PI3-kinase inhibitor. Osteocalcin, an osteoblast-specific protein whose expression corresponds with osteoblast differentiation, was increased in a dose- and time-dependent manner after insulin treatment, whereas it was decreased with IGF-1 treatment. Moreover, insulin treatment dramatically induced osteocalcin promoter activity, whereas IGF-1 treatment significantly inhibited it, indicating direct effect of insulin on osteocalcin synthesis.

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Section: Discussionmentioning

confidence: 99%

Effects of insulin and insulin‐like growth factor 1 on osteoblast proliferation and differentiation: differential signalling via Akt and ERK

Zhang

Shen

Wan

et al. 2012

Cell Biochemistry & Function

111

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“…Increased ALP activity within matrix vesicles is a prerequisite for mineral deposition [see reviews by Balcerzak et al (2003) and Boyan et al (2003)]. We therefore measured ALP activity in the different cellular compartments to assess whether these increases in ALP were linked to enhanced differentiation.…”

Section: Chlorate Induces Short-and Mid-term Disruption Of Mg-63 Prolmentioning

confidence: 99%

De‐sulfation of MG‐63 cell glycosaminoglycans delays in vitro osteogenesis, up‐regulates cholesterol synthesis and disrupts cell cycle and the actin cytoskeleton

Kumarasuriyar

Lee

Nurcombe

et al. 2009

Journal Cellular Physiology

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Glycosaminoglycan (GAG) sugars are largely responsible for the bioactivity of the proteoglycan proteins they decorate, and are particularly important for mediating the processes of cell attachment and growth factor signaling. Here, we show that chlorate-induced de-sulfation of GAGs expressed by MG-63 osteosarcoma cells results in delayed cell proliferation when the cells are exposed to chlorate for short or medium periods, but a disrupted mineralization without altered cell proliferation in response to long-term chlorate exposure. Analysis of GAG-binding growth factor activity indicated that chlorate disrupted BMP2/noggin signaling, but not FGF2 activity. Microarray analyses, which were confirmed by subsequent cell-based assays, indicated that chlorate predominantly disrupted the cell cycle and actin cytoskeleton and upregulated cholesterol synthesis, without affecting cell migration or attachment. Furthermore, we observed that disruption of the functions of the proteoglycan syndecan-4 replicated phenotypes induced by chlorate, implicating a primary role for this proteoglycan in providing bioactivity for these cells. J. Cell. Physiol. 219: 572-583, 2009. (c) 2009 Wiley-Liss, Inc.

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“…Extracellular PPi accumulation is regulated by a transmembrane protein progressive ankylosis (ANK) for extracellular channeling, nucleotide pyrophosphatase/phosphodiesterase 1 (NPP1) for generation from nucleoside triphosphates, and tissue‐nonspecific alkaline phosphatase (TNAP) for hydrolyzation (4–6).…”

mentioning

confidence: 99%

Akt1 in murine chondrocytes controls cartilage calcification during endochondral ossification under physiologic and pathologic conditions

Fukai¹,

Kawamura²,

Saito³

et al. 2010

Arthritis & Rheumatism

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Objective. To examine the role of the phosphoinositide-dependent serine/threonine protein kinase Akt1 in chondrocytes during endochondral ossification.Methods. Skeletal phenotypes of homozygous Akt1-deficient (Akt1 ؊/؊ ) mice and their wild-type littermates were compared in radiologic and histologic analyses. An experimental osteoarthritis (OA) model was created by surgically inducing instability in the knee joints of mice. For functional analyses, we used primary costal and articular chondrocytes from neonatal mice and mouse chondrogenic ATDC5 cells with retroviral overexpression of constitutively active Akt1 or small interfering RNA (siRNA) for Akt1.Results. Among the Akt isoforms (Akt1, Akt2, and Akt3), Akt1 was the most highly expressed in chondrocytes, and the total level of Akt protein was decreased in Akt1 ؊/؊ chondrocytes, indicating a dominant role of Akt1. Akt1 ؊/؊ mice exhibited dwarfism with normal proliferative and hypertrophic zones but suppressed cartilage calcification in the growth plate compared with their wild-type littermates. In mice with surgically induced OA, calcified osteophyte formation, but not cartilage degradation, was prevented in the Akt1 ؊/؊ joints. Calcification was significantly suppressed in cultures of Akt1 ؊/؊ chondrocytes or ATDC5 cells overexpressing siRNA for Akt1 and was enhanced in ATDC5 cells overexpressing constitutively active Akt1. Neither proliferation nor hypertrophic differentiation was affected by the gain or loss of function of Akt1. The expression of ANK and nucleotide pyrophosphatase/ phosphodiesterase 1, which accumulate pyrophosphate, a crucial calcification inhibitor, was enhanced by Akt1 deficiency or siRNA for Akt1 and was suppressed by constitutively active Akt1. Conclusion. Our findings indicate that Akt1 in chondrocytes controls cartilage calcification by inhibiting pyrophosphate during endochondral ossification in skeletal growth and during osteophyte formation in OA.Endochondral ossification is an essential process not only in physiologic skeletal growth, but also in pathologic disorders such as osteophyte formation during osteoarthritis (OA) progression (1,2). After chondrocytes proliferate and differentiate into mature hypertrophic cells, the cells calcify the surrounding matrix and recruit blood vessels, leading to progressive replacement of cartilage by bone. Inorganic pyrophosphate (PPi) plays a crucial role in the regulation of calcification by suppressing it through antagonizing the ability of inorganic phosphate (Pi) ions to crystallize with calcium (3).Extracellular PPi accumulation is regulated by a transmembrane protein progressive ankylosis (ANK) for extracellular channeling, nucleotide pyrophosphatase/ phosphodiesterase 1 (NPP1) for generation from nucle-

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The roles of annexins and alkaline phosphatase in mineralization process.

Cited by 182 publications

References 162 publications

Effects of insulin and insulin‐like growth factor 1 on osteoblast proliferation and differentiation: differential signalling via Akt and ERK

Effects of insulin and insulin‐like growth factor 1 on osteoblast proliferation and differentiation: differential signalling via Akt and ERK

De‐sulfation of MG‐63 cell glycosaminoglycans delays in vitro osteogenesis, up‐regulates cholesterol synthesis and disrupts cell cycle and the actin cytoskeleton

Akt1 in murine chondrocytes controls cartilage calcification during endochondral ossification under physiologic and pathologic conditions

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