1998

DOI: 10.1016/s8756-3282(98)00009-x

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A Nude Mouse Model for Human Bone Formation in Unloaded Conditions

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Ranieri Cancedda

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et al.

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Cell Sources For Tissue Engineering1

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Cited by 136 publications

(119 citation statements)

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“…PCR for the core-regulatory region of the ChM-I gene was performed using DNA extracted from an immunoprecipitated DNA-protein complex using antibodies for Sp1, Sp3, or non-immune rabbit IgG (Control Ab). (17,18), and we and others (19,20) provide the evidence for the presence of bi-directional precursors, which can differentiate into either chondrogenic or osteogenic cells. In addition to the ChM-I gene, CBOS expressed a number of cartilage-related genes such as the COL2A1, COL9A1, and AGC genes (Fig.…”

Section: Discussionsupporting

confidence: 54%

Methylation in the Core-promoter Region of the Chondromodulin-I Gene Determines the Cell-specific Expression by Regulating the Binding of Transcriptional Activator Sp3

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et al. 2004

Journal of Biological Chemistry

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Chondromodulin-I (ChM-I) 1 is a 25-kDa glycoprotein originally purified from bovine epiphyseal cartilage on the basis of growth-promoting activity for chondrocytes (1) and subsequently revealed to be a potent vascular endothelial cell growth inhibitor (2). During embryonal development, the expression of the ChM-I gene is first observed in all of the cartilaginous tissues, which are composed of prehypertrophic chondrocytes (3). As the development proceeds, hypertrophic chondrocytes develop in the center of cartilaginous bone rudiments where the expression of the ChM-I gene shows a marked decrease (3). No expression of the ChM-I gene is observed in bone tissues developing after vascular invasion in the area adjacent to hypertrophic chondrocytes (3). In matured limbs, the expression of the ChM-I gene is limited to cells in the resting, proliferating, and early hypertrophic zone of the growth plate (2-4). These results suggest that the expression of the ChM-I gene is regulated strictly in a cell-and stage-related manner, although the molecular mechanisms leading to this spatiotemporal expression have not been elucidated.Osteosarcoma (OS) is defined as a sarcoma that produces a bone matrix called osteoid, suggesting that the precursor cells of OS are cells of the osteogenic lineage (5). The degree of differentiation as osteoblasts, however, differs considerably among OS ranging from tumors with a large amount of osteoid and expressing a number of bone-related genes such as alkaline phosphatase (ALP) and osteocalcin (OCN) genes, namely osteoblastic OS (OBOS), to tumors in which an osteoid is hardly seen, fibroblastic OS (FBOS) (6 -8). A particular intriguing subtype of OS is chondroblastic OS (CBOS) in which tumor cells directly produce immature cartilage in addition to osteoid (5, 9), suggesting that tumor cells in this subtype have the potential to differentiate into both osteogenic and chondrogenic cells. These clinical findings suggest that the precursor cells of OS range from mesenchymal stem cells to mature osteoblasts and that OS cells can be used as materials to investigate the regulatory mechanisms of cell-and stage-specific genes such as the ChM-I gene.Here we first analyzed the expression of the ChM-I gene in primary OS tumors and cell lines and found that the gene was expressed strongly in CBOS but not in tumors of other subtypes. This result prompted us to investigate the involvement in regulation of the expression of the ChM-I gene of an epigenetic mechanism, which has been studied extensively as the mechanism controlling the expression of cell-and stage-specific genes (10). We found that the expression of the ChM-I gene was regulated positively by a transcription factor, Sp3, and that the binding of Sp3 was regulated by the methylation status in the core-promoter region of the ChM-I gene, especially at one Sp3 binding site. EXPERIMENTAL PROCEDURESTissue Samples-Primary tumor tissues from 24 OS cases were obtained at either biopsy or resection. All were conventional high grade tumors, and histological su...

“…PCR for the core-regulatory region of the ChM-I gene was performed using DNA extracted from an immunoprecipitated DNA-protein complex using antibodies for Sp1, Sp3, or non-immune rabbit IgG (Control Ab). (17,18), and we and others (19,20) provide the evidence for the presence of bi-directional precursors, which can differentiate into either chondrogenic or osteogenic cells. In addition to the ChM-I gene, CBOS expressed a number of cartilage-related genes such as the COL2A1, COL9A1, and AGC genes (Fig.…”

Section: Discussionsupporting

confidence: 54%

Methylation in the Core-promoter Region of the Chondromodulin-I Gene Determines the Cell-specific Expression by Regulating the Binding of Transcriptional Activator Sp3

¹

,

²

,

³

et al. 2004

Journal of Biological Chemistry

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Chondromodulin-I (ChM-I) 1 is a 25-kDa glycoprotein originally purified from bovine epiphyseal cartilage on the basis of growth-promoting activity for chondrocytes (1) and subsequently revealed to be a potent vascular endothelial cell growth inhibitor (2). During embryonal development, the expression of the ChM-I gene is first observed in all of the cartilaginous tissues, which are composed of prehypertrophic chondrocytes (3). As the development proceeds, hypertrophic chondrocytes develop in the center of cartilaginous bone rudiments where the expression of the ChM-I gene shows a marked decrease (3). No expression of the ChM-I gene is observed in bone tissues developing after vascular invasion in the area adjacent to hypertrophic chondrocytes (3). In matured limbs, the expression of the ChM-I gene is limited to cells in the resting, proliferating, and early hypertrophic zone of the growth plate (2-4). These results suggest that the expression of the ChM-I gene is regulated strictly in a cell-and stage-related manner, although the molecular mechanisms leading to this spatiotemporal expression have not been elucidated.Osteosarcoma (OS) is defined as a sarcoma that produces a bone matrix called osteoid, suggesting that the precursor cells of OS are cells of the osteogenic lineage (5). The degree of differentiation as osteoblasts, however, differs considerably among OS ranging from tumors with a large amount of osteoid and expressing a number of bone-related genes such as alkaline phosphatase (ALP) and osteocalcin (OCN) genes, namely osteoblastic OS (OBOS), to tumors in which an osteoid is hardly seen, fibroblastic OS (FBOS) (6 -8). A particular intriguing subtype of OS is chondroblastic OS (CBOS) in which tumor cells directly produce immature cartilage in addition to osteoid (5, 9), suggesting that tumor cells in this subtype have the potential to differentiate into both osteogenic and chondrogenic cells. These clinical findings suggest that the precursor cells of OS range from mesenchymal stem cells to mature osteoblasts and that OS cells can be used as materials to investigate the regulatory mechanisms of cell-and stage-specific genes such as the ChM-I gene.Here we first analyzed the expression of the ChM-I gene in primary OS tumors and cell lines and found that the gene was expressed strongly in CBOS but not in tumors of other subtypes. This result prompted us to investigate the involvement in regulation of the expression of the ChM-I gene of an epigenetic mechanism, which has been studied extensively as the mechanism controlling the expression of cell-and stage-specific genes (10). We found that the expression of the ChM-I gene was regulated positively by a transcription factor, Sp3, and that the binding of Sp3 was regulated by the methylation status in the core-promoter region of the ChM-I gene, especially at one Sp3 binding site. EXPERIMENTAL PROCEDURESTissue Samples-Primary tumor tissues from 24 OS cases were obtained at either biopsy or resection. All were conventional high grade tumors, and histological su...

“…However, the underlying molecular mechanism of action of the two factors is unknown. [18][19][20] BMSCs that are expanded in the presence of FGF-2 and DEX stimulate bone formation in nude mice. 20 In some cases, such as with rat marrow stromal cells, treatment with FGF-2 and DEX decreases DNA content as compared to FGF-2 alone.…”

Section: Introductionmentioning

confidence: 99%

Enhanced Ex Vivo Expansion of Human Adipose Tissue–Derived Mesenchymal Stromal Cells by Fibroblast Growth Factor-2 and Dexamethasone

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et al. 2009

Tissue Engineering Part A

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In the present study, we investigated the ex vivo expansion of human adipose tissue-derived mesenchymal stromal cells (ATSCs) to identify factors that promoted efficient expansion while preserving stem cell potential. We examined several growth factors and steroids, and found that the combination of a low concentration of fibroblast growth factor-2 (FGF-2) (1 ng=mL) and dexamethasone (DEX) or betamethasone (BET) enhanced the proliferation of ATSCs by approximately 30-60% as compared to control. Enhanced proliferation under these conditions was confirmed using ATSCs isolated from three independent donors. ATSCs that were expanded in the presence of FGF-2 and DEX for 5 days were capable of differentiating into either osteoblastic or adipogenic cells, and the cells were positive for the mesenchymal stem cell markers such as CD29, CD44, CD90, CD105, and CD146, suggesting that the stem cell potential of the ATSCs was preserved. Analysis of signaling pathway revealed that tyrosine phosphorylation of Src kinase was dramatically increased in response to FGF-2 and DEX, suggesting the involvement of Src-dependent pathways in the stimulatory mechanism of proliferation of ATSCs by FGF-2 and DEX. Moreover, Src family kinase inhibitors (SU6656 and Src kinase inhibitor I) substantially reduced the FGF-2 and DEX-induced proliferation of ATSCs. SU6656 also inhibited the osteogenic and adipogenic differentiation of ATSCs. The results of the current study demonstrate that FGF-2 in combination with DEX stimulates the proliferation and osteoblastic and adipogenic differentiation of ATSCs through a Src-dependent mechanism, and that FGF-2 and DEX promote the efficient ex vivo expansion of ATSCs.

“…We selected the ectopic mouse model of bone regeneration, in which human bone marrow-derived MSCs seeded on a suitable ceramic scaffold are subcutaneously implanted in the back immunocompromised mice. 31 In particular, we investigated whether the treatment with anti-21A RNAs induced differences in bone formation in terms of quantity and/or quality of the engineered tissue. Considering that the treatment with anti-21A RNAs resulted in a 1.8-fold increase in the number of MSCs, we seeded the scaffolds with two different amounts of cells: i) 2 £ 10 6 non-transfected MSCs (standard cell concentration in this type of assay); ii) 1.17 £ 10 6 for anti-21A transfected and non-transfected control MSCs (resulting from the ratio between the standard cell concentration and the population doubling increase induced by anti-21A RNAs).…”

Section: Resultsmentioning

confidence: 99%

Down-regulation of 21A Alu RNA as a tool to boost proliferation maintaining the tissue regeneration potential of progenitor cells

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et al. 2016

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ABSTRACT21A is an Alu non-coding (nc) RNA transcribed by RNA polymerase (pol) III. While investigating the biological role of 21A ncRNA we documented an inverse correlation between its expression level and the rate of cell proliferation. The downregulation of this ncRNA not only caused a boost in cell proliferation, but was also associated to a transient cell dedifferentiation, suggesting a possible involvement of this RNA in cell dedifferentiation/reprogramming. In this study, we explored the possibility to enhance proliferation and dedifferentiation of cells of interest, by 21A down-regulation, using a mixture of chemically modified Anti-21A RNAs. Our results confirmed the validity of this approach that allows the amplification of specific cell populations, in a controlled manner and without inducing permanent effects. In addition to induce cell proliferation, the procedure did not decrease the tissue regeneration potential of progenitor cells in two different cell systems.

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