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首页> 外文期刊>Cell and Tissue Research >Differential regulation of cellular maturation in chondrocytes and osteoblasts by glycine.
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Differential regulation of cellular maturation in chondrocytes and osteoblasts by glycine.

机译：甘氨酸对软骨细胞和成骨细胞中细胞成熟的差异调节。

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摘要

Previous studies have demonstrated the functional expression, by osteoblasts, of N-methyl-D-aspartate (NMDA) receptors responsible for the promotion of cellular differentiation in bone. We have now evaluated the possible role of the endogenous co-agonist of NMDA receptors, glycine (Gly), in chondrogenesis. In ex vivo organotypic cultures of fetal mouse tibias, proximal and distal cartilaginous primordia were significantly increased in the presence of Gly, with the osteogenic center being unchanged. Exposure to Gly drastically increased mRNA expression of the calcified chondrocyte marker osteopontin, without markedly affecting that of a proliferating chondrocyte marker or a hypertrophic chondrocyte marker, as shown in organotypic cultures by in situ hybridization analysis. Gly significantly increased Ca(2+) accumulation, osteopontin mRNA expression, and alkaline phosphatase activity in cultured rat costal chondrocytes, without significantly affecting those in cultured rat calvarial osteoblasts. The increase induced by Gly was significantly prevented by an NMDA receptor channel blocker and an antagonist at the Gly site on NMDA receptors, but not by an inhibitory Gly receptor antagonist or a Gly transporter inhibitor, in cultured chondrocytes. Constitutive mRNA expression was seen for NR1, NR2D, and NR3A subunits of NMDA receptors, but not for Gly receptors and transporters, in cultured chondrocytes. Corresponding immunoreactive proteins were detected for NR1 and NR2D subunits in cartilaginous zones of fetal mouse tibias. Thus, Gly might, at least in part, play a role as a trophic factor in the mechanisms associated with chondral calcification through the Gly site of NMDA receptors functionally expressed by chondrocytes in rodent cartilage.
机译：先前的研究表明成骨细胞功能性表达N-甲基-D-天冬氨酸（NMDA）受体，负责促进骨细胞分化。现在，我们已经评估了NMDA受体甘氨酸（Gly）的内源性协同激动剂在软骨形成中的可能作用。在胎儿小鼠胫骨的离体器官型培养中，在Gly存在的情况下，近端和远端软骨原基明显增加，而成骨中心没有改变。暴露于Gly可使钙化的软骨细胞标志物骨桥蛋白的mRNA表达急剧增加，而对增殖的软骨细胞标志物或肥大性软骨细胞标志物的表达无明显影响，如通过原位杂交分析在器官型培养物中显示的那样。甘氨酸显着增加Ca（2+）积累，骨桥蛋白mRNA表达和培养的大鼠肋软骨细胞中的碱性磷酸酶活性，而不会显着影响培养的大鼠颅骨成骨细胞中的钙。在培养的软骨细胞中，NMDA受体通道阻滞剂和NMDA受体上Gly位点的拮抗剂可显着阻止Gly诱导的增加，但抑制性Gly受体拮抗剂或Gly转运蛋白抑制剂则不能。在培养的软骨细胞中，NMDA受体的NR1，NR2D和NR3A亚基可见组成型mRNA表达，而Gly受体和转运蛋白则无此表达。在胎儿小鼠胫骨的软骨区中检测到了相应的免疫反应蛋白，用于检测NR1和NR2D亚基。因此，在通过啮齿类软骨细胞由软骨细胞功能性表达的NMDA受体的Gly位点与软骨钙化相关的机制中，Gly可能至少部分地充当营养因子。

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