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首页> 外文期刊>Journal of Cellular Physiology >Osterix/Sp7 regulates mesenchymal stem cell mediated endochondral ossification.
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Osterix/Sp7 regulates mesenchymal stem cell mediated endochondral ossification.

机译：Osterix / Sp7调节间充质干细胞软骨内骨化介导的。

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摘要

We investigated the expression and regulation of the zinc finger protein Osterix (Osx) during endochondral ossification in mice. In studies to determine the temporal and spatial regulation of Osx mRNA and protein during embryogenesis we found it to be present throughout development, but its expression is restricted to the immature chondro/osteoprogenitor cells and mature osteoblasts, excluding hypertrophic chondrocytes. Using a fracture model, we show a consistent pattern of Osx protein expression in mesenchymal progenitor cells in the periosteum and immature chondrocytes and osteoblasts embedded in the fracture callus. In contrast, hypertrophic chondrocytes, vessels and fibrous tissue were devoid of Osx expression. Additionally, using RNA isolated from fracture callus throughout the healing process, we observe that Osx transcripts parallel that of Runx2 and differentially overlap both cartilage and bone phenotypic markers. Furthermore, using limb bud-derived MLB13MYC Clone 17 cells, we show that PTHrPinhibited chondrocyte maturation while it enhanced mRNA levels of Osx in these chondro/osteoprogenitor cells. Gain and loss of function of Osx function experiments with these cells demonstrated that Osx serves as an inhibitor of chondrogenesis and chondrocyte maturation, while it promotes osteoblast maturation. Together, our findings provide the first demonstration of the molecular mechanisms underlying Osx inhibition of chondrocyte differentiation, and further suggest a role for this transcription factor in mediating endochondral ossification during bone repair.
机译：我们调查的表达和调控锌指蛋白Osterix (Osx)期间在小鼠软骨内成骨。确定的时间和空间规定在胚胎发生我们Osx信使rna和蛋白质发现它存在在发展,但其表达仅限于不成熟chondro / osteoprogenitor细胞和成熟成骨细胞,不包括肥厚性软骨细胞。使用骨折模型,我们将展示一种一致的的Osx的间叶细胞蛋白表达模式祖细胞在骨膜和不成熟软骨细胞和成骨细胞中嵌入骨折愈伤组织。软骨细胞、血管和纤维组织缺乏Osx的表达式。从断裂愈伤组织在孤立治疗过程中,我们观察到Osx记录平行Runx2和不同重叠软骨和骨表型标记。此外,使用肢体bud-derived MLB13MYC17细胞克隆,我们表明,PTHrPinhibited软骨细胞的成熟而增强mRNA在这些chondro / osteoprogenitor Osx的水平细胞。实验表明,与这些细胞Osx作为软骨形成的抑制剂软骨细胞的成熟,它促进成骨细胞成熟。提供第一个示范的分子机制Osx的抑制软骨细胞分化,并进一步建议这种转录因子调节的作用在骨修复软骨内成骨。

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