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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Nuclear receptor chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) modulates mesenchymal cell commitment and differentiation
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Nuclear receptor chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) modulates mesenchymal cell commitment and differentiation

机译：核受体鸡卵清蛋白上游启动子转录因子II（COUP-TFII）调节间充质细胞的承诺和分化。

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摘要

The mesenchymal cell is a multipotent stem cell with the capacity to give rise to multiple cell types such as adipocytes, osteoblasts, chondrocytes, and myocytes. However, the molecular events responsible for their lineage specification and differentiation remain obscure. Here we show that inactivation of chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII), a member of the nuclear receptor superfamily, in mesenchymal progenitors favors osteoblast and myoblast development while simultaneously impairing adipogenic and chondrogenic programs. During mouse embryogenesis, COUP-TFII protein is highly detected in the mesenchymal compartment and is involved in mesoderm tissue formation. Ablation of COUP-TFII in mice led to higher bone density, increased muscle mass, and suppression of cartilage and fat formation. We further demonstrate that COUP-TFII directs the plasticity of mesenchymal precursors primarily through the combined modulation of Wnt signaling, Runx2 activity, as well as PPARy and Sox9 expression. Together, our results provide insight into the mechanisms whereby a single nuclear receptor can fine-tune the lineage-specific differentiation of a progenitor cell.
机译：间充质细胞是一种多能干细胞，具有产生多种细胞类型的能力，例如脂肪细胞，成骨细胞，软骨细胞和肌细胞。但是，负责其谱系规格和分化的分子事件仍然不清楚。在这里，我们显示间质祖细胞中鸡卵清蛋白上游启动子转录因子II（COUP-TFII）的失活，促进间充质祖细胞和成肌细胞的发育，同时损害成脂和成软骨程序。在小鼠胚胎发生过程中，在间质隔室中高度检测到了COUP-TFII蛋白，并参与了中胚层组织的形成。小鼠中COUP-TFII的消融导致更高的骨密度，增加的肌肉质量以及抑制软骨和脂肪形成。我们进一步证明，COUP-TFII主要通过对Wnt信号，Runx2活性以及PPARy和Sox9表达的组合调节来指导间充质前体的可塑性。在一起，我们的结果提供了对单个核受体可以微调祖细胞的谱系特异性分化的机制的见解。

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    Xin Xie; Jun Qin; Sue-Hwa Lin; Sophia Y. Tsai; Ming-Jer Tsai;

  • 作者单位

    Department of Molecular and Cellular Biology;

    Department of Molecular and Cellular Biology;

    Departments of Molecular Pathology and Genitourinary Medical Oncology, University of Texas MD Anderson Cancer Center, Houston, TX 77030;

    Department of Molecular and Cellular Biology,Program in Developmental Biology,Department of Medicine, Baylor College of Medicine, Houston, TX 77030;

    Department of Molecular and Cellular Biology,Program in Developmental Biology,Department of Medicine, Baylor College of Medicine, Houston, TX 77030;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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