Regulation of osteocalcin secretion by human primary bone cells and by the human osteosarcoma cell line MG-63

Kiebzak, Gary M.; Frondoza, Carmelita G.; Sacktor, Bertram

doi:10.1016/0169-6009(91)90025-u

Cited by 85 publications

(82 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The MG63 cell line has been well characterized showing numerous osteoblastic features, including the expression of BMP (Virdi et al, 1998), alkaline phosphatase Lincks et al, 1998), Cbfa-1 (SasakiIwaoka et al, 1999 as well as osteocalcin (Lajeunesse et al, 1990;Kue et al, 1999). However, in agreement with Boyan et al (2002), we have failed to detect the production of osteocalcin or alkaline phosphatase, even after stimulation by either Vitamin D or dexamethazone (data not shown).…”

Section: Discussioncontrasting

confidence: 33%

“…To achieve this goal, we have used the human osteoblast-like cell line MG63 as the cellular prototype (Billiau et al, 1975). This cell line, originally isolated from a human osteosarcoma, has been well characterized (Lajeunesse et al, 1990;1991) and largely used in biocompatibility tests (Lohmann et al, 1999;Lincks et al, 1998;Martin et al, 1995). In our study, we used either 45S5 â BG granules, or 45S5 granules conditioned prior to the cultures, by incubation in tris buffer to generate the Ca-P surface layer.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Behaviour of moderately differentiated osteoblast-like cells cultured in contact with bioactive glasses

Hattar¹,

Berdal²,

Asselin³

et al. 2002

eCM

View full text Add to dashboard Cite

Bioactive glasses have been shown to stimulate osteogenesis both in vivo and in vitro. However, the molecular mechanisms underlying this process are still poorly understood. In this study, we have investigated the behaviour of osteoblast-like cells (MG63), cultured in the presence of bioglass particles. Three types of granules were used: 45S5 ® bioactive glass, 45S5 ® granules preincubated in tris buffer and 60S non-reactive glass, used as control. Phase contrast microscopy permitted step-by-step visualization of cell cultures in contact with the particles. Ultrastructural observations of undecalcified sections revealed direct contacts of the cells and an electron-dense layer located at the periphery of the material. Protein synthesis was evaluated biochemically and showed a gradual increase throughout the culture time in the three types of cultures. Alkaline phosphatase was detected in situ, in clusters of packed cells either in contact with the material or in the background cell layer. Semi-quantitative RT-PCR analysis of the main osteoblastic markers showed that gene expression was maintained in all three cultures. The fact that osteocalcin was not detected, supports the fact that the MG63 cell line is composed of less differentiated osteogenic cells rather than mature osteoblasts. We also demonstrated for the first time in this cell line, the expression of Msx-2, Dlx-3 and Dlx-7 homeogenes, known to regulate in vivo foetal skeletogenesis as well as adult skeletal regeneration. However, no significant differences could be recognised in the expression pattern of bone markers between the three types of cultures. Yet these preliminary results indicate that bioactive glasses provided a suitable environment for the growth and proliferation of osteoblasts in vitro, since no drastic changes in phenotype expression of pre-osteoblasts was noted.

show abstract

Section: Discussioncontrasting

confidence: 33%

Section: Introductionmentioning

confidence: 99%

Behaviour of moderately differentiated osteoblast-like cells cultured in contact with bioactive glasses

Hattar¹,

Berdal²,

Asselin³

et al. 2002

eCM

View full text Add to dashboard Cite

show abstract

“…Isolation of the subchondral bone plate and the cell cultures were performed as previously described (1,15,24,25). Briefly, the overlaying cartilage was first removed from tibial plateaus, and the trabecular bone tissue was dissected away from the subchondral bone plate.…”

Section: Methodsmentioning

confidence: 99%

“…Confluent cells were then incubated in the presence or absence of 1,25-dihydroxyvitamin D 3 (1,25[OH] 2 D 3 ) (50 nM) for 48 hours for the determination of biomarkers or in presence of 0.5% bovine serum albumin (BSA) for the determination of prostaglandins, cytokines, and collagen. Supernatants were collected at the end of the incubation period and kept at Ϫ80°C prior to performance of the assays.…”

Section: Methodsmentioning

confidence: 99%

Altered mineralization of human osteoarthritic osteoblasts is attributable to abnormal type I collagen production

Couchourel

Aubry

Delalandre

et al. 2009

Arthritis & Rheumatism

Self Cite

130

119

View full text Add to dashboard Cite

Objective. Bone tissue in osteoarthritis (OA) is composed of abundant undermineralized osteoid matrix. The aim of this study was to investigate the mechanisms responsible for this abnormal matrix, using in vitro OA subchondral osteoblasts.Methods. Primary normal and OA osteoblasts were prepared from tibial plateaus. Phenotype was determined by alkaline phosphatase activity, and osteocalcin, osteopontin, prostaglandin E 2 (PGE 2 ), and transforming growth factor ␤1 (TGF␤1) were assessed by enzyme-linked immunosorbent assay. Expression of COL1A1 and COL1A2 was determined by real-time polymerase chain reaction. The production of type I collagen was determined by the release of its C-terminal propeptide and Western blot analysis. In vitro mineralization was evaluated by alizarin red staining. Inhibition of TGF␤1 expression was performed using a small interfering RNA technique.Results. Mineralization of OA osteoblasts was reduced compared with mineralization of normal osteoblasts, even in the presence of bone morphogenetic protein 2 (BMP-2). Alkaline phosphatase and osteocalcin levels were elevated in OA osteoblasts compared with normal osteoblasts, whereas osteopontin levels were similar. The COL1A1-to-COL1A2 messenger RNA ratio was 3-fold higher in OA osteoblasts compared with normal osteoblasts, and the production of collagen by OA osteoblasts was increased. Because TGF␤1 inhibits BMP-2-dependent mineralization, and because TGF␤1 levels are ϳ4-fold higher in OA osteoblasts than in normal osteoblasts, inhibiting TGF␤1 levels in OA osteoblasts corrected the abnormal COL1A1-to-COL1A2 ratio and increased alizarin red staining.Conclusion. Elevated TGF␤1 levels in OA osteoblasts are responsible, in part, for the abnormal ratio of COL1A1 to COL1A2 and for the abnormal production of mature type I collagen. This abnormal COL1A1-to-COL1A2 ratio generates a matrix that blunts mineralization in OA osteoblasts.

show abstract

“…Human primary bone cell cultures were prepared as previously described (25) from bone biopsies of normal individuals, pre-BMT for EC and MG, and 2 yr post-BMT for EC (bone marrow transplant was successful for patient MG as assessed at the 3-mo follow-up, but MG died 6 mo post-BMT of pulmonary restriction). Briefly, bone explants were washed free of blood, and trabecular bone was cut out of surrounding cortical bone and minced in 2 mm 2 pieces.…”

Section: Methodsmentioning

confidence: 99%

Demonstration of an osteoblast defect in two cases of human malignant osteopetrosis. Correction of the phenotype after bone marrow transplant.

Lajeunesse¹,

Busque²,

Ménard³

et al. 1996

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

Regulation of osteocalcin secretion by human primary bone cells and by the human osteosarcoma cell line MG-63

Cited by 85 publications

References 23 publications

Behaviour of moderately differentiated osteoblast-like cells cultured in contact with bioactive glasses

Behaviour of moderately differentiated osteoblast-like cells cultured in contact with bioactive glasses

Altered mineralization of human osteoarthritic osteoblasts is attributable to abnormal type I collagen production

Demonstration of an osteoblast defect in two cases of human malignant osteopetrosis. Correction of the phenotype after bone marrow transplant.

Contact Info

Product

Resources

About