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MG63 Cells (mg63 + cell)
Selected AbstractsExtracts Of Actinobacillus Actinomycetemcomitans Induce Apoptotic Cell Death In Human Osteoblastic MG63 CellsAUSTRALIAN ENDODONTIC JOURNAL, Issue 1 2000Article first published online: 11 FEB 2010 No abstract is available for this article. [source] Effects of Antrodia camphorata on viability, apoptosis, [Ca2+]i, and MAPKs phosphorylation in MG63 human osteosarcoma cellsDRUG DEVELOPMENT RESEARCH, Issue 2 2007Yih-Chau Lu Abstract The present study explored the effect of Antrodia camphorata (AC) on viability, apoptosis, mitogen-activated protein kinases (MAPKs) phosphorylation, and Ca2+ regulation in MG63 human osteosarcoma cells. AC (25,50,µg/ml) did not affect cell viability, but at 100,200,µg/ml decreased viability and induced apoptosis in a concentration-dependent manner. AC at concentrations of 25,200,µg/ml did not alter basal [Ca2+]i, but at 25,µg/ml decreased [Ca2+]i increases induced by ATP, bradykinin, histamine, and thapsigargin. ATP, bradykinin, and histamine increased cell viability while thapsigargin decreased it. AC (25,µg/ml) pretreatment failed to alter bradykinin- and thapsigargin-induced effects on viability, but potentiated ATP- and histamine-induced increases in viability. Immunoblotting showed that MG63 cells did not have background phospho-JNK and phospho-p38 mitogen-activated protein kinases (MAPKs); and AC did not induce the phosphorylation of these two MAPKs. Conversely, the cells had significant background phospho-ERK MAPK that was inhibited by 200,µg/ml AC. The ERK-specific inhibitor PD98059 also induced cell death. Collectively, in MG63 cells, AC exerted multiple effects on viability and [Ca2+]i, caused apoptosis probably via inhibition of ERK MAPK phosphorylation. Drug Dev Res 68:71,78, 2007. © 2007 Wiley-Liss, Inc. [source] 2-methoxyestradiol-induced cell death in osteosarcoma cells is preceded by cell cycle arrestJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 5 2008Avudaiappan Maran Abstract 2-Methoxyestradiol (2-ME), a naturally occurring mammalian metabolite of 17,-Estradiol (E2), induces cell death in osteosarcoma cells. To further understand the molecular mechanisms of action, we have investigated cell cycle progression in 2-ME-treated human osteosarcoma (MG63, SaOS-2 and LM8) cells. At 5 µM, 2-ME induced growth arrest by inducing a block in cell cycle; 2-ME-treatment resulted in 2-fold increases in G1 phase cells and a decrease in S phase cells in MG63 and SaOS-2 osteosarcoma cell lines, compared to the appropriate vehicle controls. 2-ME-treatment induced a threefold increase in the G2 phase in LM8 osteosarcoma cells. The results demonstrated steroid specificity, as the tumorigenic metabolite, 16,-hydroxyestradiol (16-OHE), did not have any effect on cell cycle progression in osteosarcoma cells. The cell cycle arrest coincided with an increase in expression of the cell cycle markers p21, p27 and p53 proteins in 2-ME-treated osteosarcoma cells. Also, MG63 cells, transiently transfected with cDNA for a ,loss of function mutant' RNA-dependent protein kinase (PKR) protein, were resistant to 2-ME-induced cell cycle arrest. These results suggest that 2-ME works in concert with factors regulating cell cycle progression, and cell cycle arrest precedes cell death in 2-ME-treated osteosarcoma cells. J. Cell. Biochem. 104: 1937,1945, 2008. © 2008 Wiley-Liss, Inc. [source] Further characterization of human fetal osteoblastic hFOB 1.19 and hFOB/ER, cells: Bone formation in vivo and karyotype analysis using multicolor fluorescent in situ hybridizationJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 1 2002M. Subramaniam Abstract We have previously generated an immortalized human fetal osteoblastic cell line (hFOB) using stably transfected temperature sensitive SV40 T-antigen (Harris et al. [1995a] J. Bone. Miner. Res. 10:178,1860). To characterize these cells for phenotypic/genotypic attributes desired for a good cell model system, we performed karyotype analysis by multicolor fluorescent in situ hybridization (M-FISH), their ability to form bone in vivo without developing cell transformation, and finally their ability to form extracellular matrix formation in vitro. The karyotype analysis of hFOB cells revealed structural or numeric anomalies involving 1,2 chromosomes. In contrast, the human osteosarcoma MG63 cells displayed multiple, and often complex, numeric, and structural abnormalities. Subcutaneous injection of hFOB cells in the presence of Matrigel into nude mice resulted in bone formation after 2,3 weeks. Electron microscopic analysis of the extracellular matrix deposited by hFOB cells in culture revealed a parallel array of lightly banded fibrils typical of the fibrillar collagens such as type I and III. These results demonstrate that the hFOB cell line has minimal chromosome abnormalities, exhibit the matrix synthetic properties of differentiated osteoblasts, and are immortalized but non-transformed cell line. These hFOB cells thus appear to be an excellent model system for the study of osteoblast biology in vitro. J. Cell. Biochem. 87: 9,15, 2002. © 2002 Wiley-Liss, Inc. [source] Subculture affects the phenotypic expression of human periodontal ligament cells and their response to fibroblast growth factor-2 and bone morphogenetic protein-7,in vitroJOURNAL OF PERIODONTAL RESEARCH, Issue 5 2008S. Lossdörfer Background and Objective:, Although periodontal ligament cells display several osteoblastic traits, their phenotypic expression is still not well established. It remains a matter of debate whether they resemble a terminally differentiated cell type or an intermediate maturation state that potentially can be directed towards a fibroblastic or an osteoblastic phenotype. Material and Methods:, To explore the characteristics of periodontal ligament cells in greater detail, fourth-passage, sixth-passage and eighth-passage human periodontal ligament cells were cultured for up to 3 wk. Ki-67, alkaline phosphatase, osteocalcin, osteoprotegerin and receptor activator of nuclear factor-,B ligand (RANKL) mRNA expression was quantified by real-time polymerase chain reaction. Furthermore, the cellular response to fibroblast growth factor-2 and bone morphogenetic protein-7 was examined in first-passage and fourth-passage cells. Dermal fibroblasts (1BR.3.G) and osteoblast-like cells (MG63) served as reference cell lines. Results:, Proliferation decreased over time and was highest in fourth-passage cells. The expression of differentiation parameters, osteoprotegerin and RANKL increased with culture time and was higher in fourth-passage cells than in cells of later passages. The RANKL/osteoprotegerin ratio increased steadily until day 21. Administration of fibroblast growth factor-2 enhanced cell numbers in both passages, whereas alkaline phosphatase and osteocalcin production remained unchanged. By contrast, exposure of periodontal ligament cells to bone morphogenetic protein-7 resulted in a reduction of cell number in the first and fourth passages, whereas the production of alkaline phosphatase and osteocalcin was enhanced. In dermal fibroblasts, differentiation parameters did not respond to both stimuli. MG63 cells behaved similarly to periodontal ligament cells. Conclusion:, These results indicate that subculture affects the phenotypic expression of human periodontal ligament cells with respect to the characteristics that these cells share with osteoblasts. Furthermore, the periodontal ligament cell phenotype can be altered by fibroblastic and osteoblastic growth factors. [source] The role of the calmodulin-dependent pathway in static magnetic field-induced mechanotransduction,BIOELECTROMAGNETICS, Issue 4 2010Jen-Chang Yang Abstract While the effects of static magnetic fields (SMFs) on osteoblastic differentiation are well demonstrated, the mechanotransduction pathways of SMFs are still unclear. The aim of this study was to explore the role of calmodulin in the biophysical effects of SMFs on osteoblastic cells. MG63 cells were exposed to a 0.4,T SMF. The expression of phosphodiesterase RNA in the cytoplasm was tested using real-time polymerase chain reaction. The differentiation of the cells was assessed by detecting changes in alkaline phosphatase activity. The role of calmodulin antagonist W-7 was used to evaluate alterations in osteoblastic proliferation and differentiation after the SMF simulations. Our results showed that SMF exposure increased alkaline phosphatase activity and phosphodiesterase 1C gene expression in MG63 cells. Addition of W-7 significantly inhibited the SMF-induced cellular response. We suggest that one possible mechanism by which SMFs affects osteoblastic maturation is through a calmodulin-dependent mechanotransduction pathway. Bioelectromagnetics 31:255,261, 2010. © 2009 Wiley-Liss, Inc. [source] Differential expression of protein phosphatase type 1 isotypes and nucleolin during cell cycle arrestCELL BIOCHEMISTRY AND FUNCTION, Issue 4 2007Hiroyuki Morimoto Abstract In the present study, we examined the expression and cytolocalization of protein phosphatase type 1 (PP1) isoforms and nucleolin in human osteoblastic cell line MG63 cells at two boundaries in the cell cycle. We treated MG63 cells with hydroxyurea and nocodazole to arrest the cells at the G1/S and G2/M boundaries, respectively. As judged from the results of Western blot analysis, PP1 isoforms were expressed differently at each boundary of the cell cycle. Nucleolin was also shown to have a different expression pattern at each boundary. In the hydroxyurea-treated cells, nucleolus-like bodies were bigger in size and decreased in number compared with those in asynchronized cells. However, the subcellular localization of PP1s and nucleolin was not changed. Anti-nucleolin antibody interacted with 110-kDa and 95-kDa proteins present in asynchronized cells and in the cells treated with hydroxyurea. Treatment of the cells with nocodazole decreased the level of the 95-kDa form of nucleolin. In the nocodazole-treated cells, it was impossible to distinguish the distribution of each protein. The phosphorylation status of nucleolin in the cell cycle arrested samples was examined by 2D,IEF,PAGE followed by Western blot analysis. In the case of asynchronized cells or hydroxyurea-treated ones, nucleolin was located at a basic isoelectric point (dephosphorylated status); whereas in the G2/M arrest cells, the isoelectric point of nucleolin shifted to an acidic status, indicating that nucleolin was phosphorylated. The present results indicate that PP1 and nucleolin were differently expressed at G1/S and G2/M boundaries of the cell cycle and acted in a different fashion during cell-cycle progression. Copyright © 2005 John Wiley & Sons, Ltd. [source] | |||||||||||||