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首页> 外文期刊>Journal of Cellular Physiology >Retinoic acid stimulates the transcription of insulin-like growth factor binding protein-6 in skeletal cells.
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Retinoic acid stimulates the transcription of insulin-like growth factor binding protein-6 in skeletal cells.

机译：视黄酸刺激的转录胰岛素样生长因子结合protein-6骨骼细胞。

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摘要

Retinoic acid has important actions on cell differentiation and osteoblastic function, and some of these actions may be mediated by changes in the insulin-like growth factor (IGF) axis. Skeletal cells synthesize IGF I and II and the six known IGF binding proteins (IGFBP). IGFBP-6 binds IGF II with high affinity and prevents IGF II-mediated effects. In fibroblasts, IGFBP-6 levels are regulated by retinoic acid, and we postulated that retinoic acid may regulate IGF II in bone by altering IGFBP-6 synthesis. We examined the effect of retinoic acid on IGFBP-6 expression in cultures of osteoblast-enriched cells from 22-day fetal rat calvariae (Ob cells). Retinoic acid caused a time- and dose-dependent increase in IGFBP-6 mRNA levels, as determined by Northern blot analysis. The effect was maximal after 48 h of treatment and observed with retinoic acid at concentrations of 10 nM to 1 microM. Retinoic acid increased IGFBP-6 polypeptide levels in the culture medium, as determined by Western immunoblot analysis.Cycloheximide at 3.6 microM slightly decreased IGFBP-6 transcripts but did not prevent the stimulatory effect of retinoic acid. The decay of IGFBP-6 mRNA in transcriptionally arrested Ob cells was similar in control and retinoic acid-treated cells, and retinoic acid increased the rates of IGFBP-6 transcription, as determined by nuclear run on assays. In conclusion, retinoic acid enhances IGFBP-6 expression in Ob cells by transcriptional mechanisms. Since IGFBP-6 prevents the effects of IGF II, increased synthesis of IGFBP-6 could mediate selected actions of retinoic acid in bone.
机译：视黄酸对细胞具有重要操作分化和成骨细胞的功能其中的一些行为可能是由变化胰岛素样生长因子(IGF)轴。骨骼细胞合成IGF I和II和6个已知IGF结合蛋白(IGFBP)。与高亲和力和防止IGF结合IGF IIII-mediated效果。水平是由视黄酸,我们假定视黄酸可能调节IGF II在骨通过改变IGFBP-6合成。检查IGFBP-6视黄酸的影响osteoblast-enriched表达文化22天细胞从胎鼠calvariae (Ob细胞)。维甲酸造成时间和剂量依赖性增加IGFBP-6 mRNA水平,由北部污点分析。经过48小时的治疗和观察视黄酸浓度的10 nM为1microM。培养基中多肽含量,由西方免疫印迹分析。减少IGFBP-6记录但没有阻止视黄酸的刺激效应。衰变IGFBP-6信使rna的转录在控制和逮捕Ob细胞相似视黄酸洗细胞和视黄酸IGFBP-6转录率的增加由核上运行分析。结论,视黄酸提高IGFBP-6通过转录表达Ob细胞机制。IGF II, IGFBP-6合成的增加调解选择行动的视黄酸骨头。

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