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首页> 外文期刊>Journal of Cellular Physiology >1α,25-dihydroxyvitamin D3 stimulates activin A production to fine-tune osteoblast-induced mineralization
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1α,25-dihydroxyvitamin D3 stimulates activin A production to fine-tune osteoblast-induced mineralization

机译：1α,25-dihydroxyvitamin D3刺激激活素A生产调整osteoblast-induced矿化

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摘要

In healthy bones, mineralization has to be tightly controlled to avoid pathological phenotypes. In this study, we investigated interactions between 1α,25(OH)2D3 (1,25D3) and activin A in the regulation of osteoblast induced mineralization. In human osteoblast cultures, we demonstrated that besides stimulation of mineralization, 1,25D3 also induced activin A, a strong inhibitor of mineralization. Simultaneously, follistatin (FST), the natural antagonist of activin A, was down-regulated by1,25D3. This resulted in an increase in activin A activity during 1,25D3 treatment. We also showed that in 1,25D3-treated osteoblasts, mineralization can be further increased when activin A activity was abrogated by adding exogenous FST. This observation implies that, besides stimulation of mineralization, 1,25D3 also controls activin A-mediated inhibition of mineralization. Besides activin A, 1,25D3 also induces osteocalcin (BGLAP), another inhibitor of mineralization. Warfarin, which has been shown to inactivate osteocalcin, increased 1,25D3-induced mineralization. Interaction between these two systems became evident from the synergistic increase in BGLAP expression upon blocking activin activity in 1,25D3-treated cultures. In conclusion, we demonstrate that 1,25D3 stimulation of mineralization by human osteoblasts is suppressed by concomitant induction of inhibitors of mineralization. Mineralization induction by 1,25D3 may actually be controlled via interplay with activin A and osteocalcin. Finally, this complex regulation of mineralization substantiates the significance of tight control of mineralization to prevent excessive mineralization and consequently reduction in bone quality and strength.
机译：在健康的骨骼,矿化必须严格控制以避免病理表型。这项研究中,我们调查之间的相互作用1α,25 (OH) 2 d3 (1,25 d3)和苯丙酸诺龙的调节成骨细胞诱导矿化。在人类成骨细胞文化中,我们演示了除了刺激的矿化,1,25 d3也诱导激活素A,一个强有力的抑制剂矿化。(置)的天然拮抗剂苯丙酸诺龙,理气by1 25 d3。提高苯丙酸诺龙活动期间1,25 d3治疗。成骨细胞矿化可以进一步当苯丙酸诺龙活动增加被废除通过添加外源性置。除了刺激的矿化,1,25 d3也控制苯丙酸诺龙一个调解的抑制矿化。1,25 d3也诱发骨钙素(BGLAP),另一个地方成矿作用的抑制剂。灭活骨钙素,增加1,25 d3-induced矿化。从这两个系统之间变得明显协同增加BGLAP表达式阻塞苯丙酸诺龙活动1,25 d3-treated文化。1,25 d3刺激人类的矿化成骨细胞是由伴随的抑制诱导矿化的抑制剂。矿化诱导的1,25 d3实际上可能通过控制相互作用与激活素A和骨钙素。矿化具体化的意义严格控制矿化的预防过度的矿化,因此减少骨质量和力量。

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