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首页> 外文期刊>Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research >In vitro demonstration of cell-to-cell interaction in growth plate cartilage using chondrocytes established from p53-/- mice.
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In vitro demonstration of cell-to-cell interaction in growth plate cartilage using chondrocytes established from p53-/- mice.

机译:使用从p53-/-小鼠建立的软骨细胞在生长板软骨中进行细胞间相互作用的体外演示。

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Three clonal cell lines (MMR14, MMR17, and MMR32) were established from the costal cartilage derived from p53-/- mice. Expression profiles of cartilage-related molecules in MMR14 and MMR17 were compatible with those in cells of the hypertrophic zone. Prolonged in vitro culture induced the expression of calcification-related genes in both cell lines, but calcified nodules were observed only in MMR14. The expression profile of cartilage-related molecules in MMR32 was compatible with that of cells in the perichondrium, with high expression levels of decorin, bone morphogenetic protein-3, and parathyroid hormone-related peptide (PTHrP). When MMR14 was co-cultured with an equal amount of MMR32 without direct contact, the nodule formation was completely inhibited, whereas no such inhibition was observed when MMR14 was co-cultured with MMR17, indicating that soluble factors produced by MMR32 were responsible for the inhibition. Blocking the effects of PTHrP by either antagonizing peptide or neutralizing antibody against PTHrP failed to rescue the inhibitory effects of MMR32, and no increase of the cyclic adenosine monophosphate production in MMR14 was observed when co-cultured with MMR32, suggesting that soluble factors other than PTHrP produced by MMR32 were responsible for the inhibition of terminal differentiation of hypertrophic chondrocytes. This report is the first to show cell-to-cell interaction in the growth plate using cell lines, which will be useful material to investigate the regulatory mechanism of chondrocyte differentiation.
机译:从来源于p53-/-小鼠的肋软骨建立了三个克隆细胞系(MMR14,MMR17和MMR32)。 MMR14和MMR17中与软骨相关的分子的表达谱与肥大区细胞中的表达谱相容。长时间的体外培养可诱导两种细胞系中钙化相关基因的表达,但仅在MMR14中观察到钙化的结节。 MMR32中软骨相关分子的表达谱与软骨膜中细胞的表达谱兼容,其中decorin,骨形态发生蛋白3和甲状旁腺激素相关肽(PTHrP)的表达水平很高。当MMR14与等量的MMR32不直接接触共培养时,结节的形成被完全抑制,而当MMR14与MMR17共培养时则没有观察到这种抑制作用,这表明由MMR32产生的可溶性因子是抑制作用的原因。 。通过拮抗肽或抗PTHrP的中和抗体来阻断PTHrP的作用未能挽救MMR32的抑制作用,与​​MMR32共培养时未观察到MMR14中环状单磷酸腺苷产生的增加,表明除PTHrP以外的可溶性因子由MMR32产生的产物负责抑制肥大软骨细胞的终末分化。该报告首次显示了使用细胞系在生长板中的细胞间相互作用,这将是研究软骨细胞分化调控机制的有用材料。

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