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首页> 外文期刊>Bone >Extracellular calcium regulates parathyroid hormone-related peptide expression in osteoblasts and osteoblast progenitor cells.
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Extracellular calcium regulates parathyroid hormone-related peptide expression in osteoblasts and osteoblast progenitor cells.

机译：细胞外钙调节成骨细胞和成骨细胞祖细胞中甲状旁腺激素相关的肽表达。

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Parathyroid hormone-related peptide (PTHrP) has been shown to have anabolic effects on bone in women with postmenopausal osteoporosis. On the cellular level PTHrP promotes the recruitment of osteogenic cells and prevents apoptotic death of osteoblasts and osteocytes. The calcium concentration is considerably higher in the vicinity of resorbing osteoclasts than in the plasma. Therefore the osteoblasts are likely to be confronted by elevated extracellular calcium concentrations in the areas of resorptive activity. The present study was designed to assess the possibility that extracellular calcium could regulate PTHrP expression in osteoblastic cells. Adult human mesenchymal stem cells (hMSC) were cultured and differentiated by standard methods. The PTHrP release into the culture media was measured by an immunoradiometric assay and the expression of PTHrP, osteocalcin and Runx2 mRNA was assayed by real-time PCR. Increasing the extracellular calcium from 1 mM to 5 mM for 24 h resulted in a 4-6-fold increase in the PTHrP release. PTHrP mRNA was also increased by elevated calcium levels. The effect of calcium stimulation on PTHrP release could be seen within 60 min of treatment. The extracellular calcium sensing receptor (CaR) agonist neomycin mimicked the effects of calcium and the MEK/MAPK inhibitor PD98059 abolished the effect of calcium and neomycin. High extracellular calcium increased the mineralization of hMSC and the expression of osteocalcin, but this effect was not mimicked by neomycin. Our results show that in hMSC, elevated extracellular calcium levels increases both released PTHrP and PTHrP mRNA expression. The effect of calcium on PTHrP can be mimicked by activation of the CaR and can be diminished by inhibition of the MAPK signalling pathway.
机译：甲状旁腺激素相关肽（PTHrP）已显示对绝经后骨质疏松症妇女的骨具有合成代谢作用。在细胞水平上，PTHrP促进成骨细胞的募集并防止成骨细胞和骨细胞的凋亡性死亡。在吸收性破骨细胞附近的钙浓度明显高于血浆中的钙浓度。因此，成骨细胞在吸收活性区域可能面临细胞外钙浓度升高的问题。本研究旨在评估细胞外钙可能调节成骨细胞中PTHrP表达的可能性。通过标准方法培养和分化成人间充质干细胞（hMSC）。通过免疫放射测定法测定释放到培养基中的PTHrP，并通过实时PCR测定PTHrP，骨钙素和Runx2 mRNA的表达。在24小时内将细胞外钙从1 mM增加到5 mM导致PTHrP释放增加4-6倍。钙水平升高也会增加PTHrP mRNA的表达。在治疗60分钟内即可看到钙刺激对PTHrP释放的影响。细胞外钙敏感受体（CaR）激动剂新霉素模仿了钙的作用，而MEK / MAPK抑制剂PD98059取消了钙和新霉素的作用。高的细胞外钙增加了hMSC的矿化作用和骨钙素的表达，但新霉素并未模仿这种作用。我们的结果表明，在hMSC中，细胞外钙水平升高会同时释放PTHrP和PTHrP mRNA表达。钙对PTHrP的作用可以通过激活CaR来模拟，并且可以通过抑制MAPK信号通路来减弱。

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