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首页> 外文期刊>Cell metabolism >Suppression of Wnt signaling by Dkk1 attenuates PTH-mediated stromal cell response and new bone formation.
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Suppression of Wnt signaling by Dkk1 attenuates PTH-mediated stromal cell response and new bone formation.

机译：Dkk1抑制Wnt信号传导减弱了PTH介导的基质细胞反应和新骨形成。

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摘要

Parathyroid hormone (PTH) suppresses Dickkopf 1 (Dkk1) expression in osteoblasts. To determine whether this suppression is essential for PTH-mediated Wnt signaling and bone formation, we examined mice that overexpress Dkk1 in osteoblasts (Dkk1 mice). Dkk1 mice were osteopenic due to abnormal osteoblast and osteoclast activity. When fed a low-calcium diet, and in two other models of hyperparathyroidism, these mice failed to develop the peritrabecular stromal cell response ("osteitis fibrosis") and new bone formation seen in wild-type mice. Despite these effects of Dkk1 overexpression, PTH still activated Wnt signaling in Dkk1 mice and in osteoblastic cells cultured from these mice. In cultured MC3T3E1 preosteoblastic cells, PTH dramatically suppressed Dkk1 expression, induced PKA-mediated phosphorylation of beta-catenin, and significantly enhanced Lef1 expression. Our findings indicate that the full actions of PTH require intact Wnt signaling but that PTH can activate the Wnt pathway despite overexpression of Dkk1.
机译：甲状旁腺激素（PTH）抑制成骨细胞中Dickkopf 1（Dkk1）的表达。为了确定这种抑制作用对于PTH介导的Wnt信号传导和骨形成是否必不可少，我们检查了成骨细胞中过表达Dkk1的小鼠（Dkk1小鼠）。 Dkk1小鼠由于成骨细胞和破骨细胞活性异常而骨质减少。当喂食低钙饮食和其他两种甲状旁腺功能亢进模型时，这些小鼠无法发展出小梁周围基质细胞反应（“骨炎性纤维化”）和在野生型小鼠中看到的新骨形成。尽管Dkk1过表达具有这些作用，但PTH仍在Dkk1小鼠和从这些小鼠培养的成骨细胞中激活Wnt信号传导。在培养的MC3T3E1前成骨细胞中，PTH显着抑制Dkk1表达，诱导PKA介导的β-catenin磷酸化，并显着增强Lef1表达。我们的发现表明，PTH的全部作用需要完整的Wnt信号传导，但尽管Dkk1过表达，PTH仍可以激活Wnt途径。

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