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首页> 外文期刊>Molecular and Cellular Biology >CTGF Mediates Smad-Dependent Transforming Growth Factor β Signaling To Regulate Mesenchymal Cell Proliferation during Palate Development
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CTGF Mediates Smad-Dependent Transforming Growth Factor β Signaling To Regulate Mesenchymal Cell Proliferation during Palate Development

机译：CTGF介导Smad依赖性转化生长因子β信号调节Pal发育期间的间充质细胞增殖。

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Transforming growth factor β (TGF-β) signaling plays crucial functions in the regulation of craniofacial development, including palatogenesis. Here, we have identified connective tissue growth factor (Ctgf) as a downstream target of the TGF-β signaling pathway in palatogenesis. The pattern of Ctgf expression in wild-type embryos suggests that it may be involved in key processes during palate development. We found that Ctgf expression is downregulated in both Wnt1-Cre; Tgfbr2fl/fl and Osr2-Cre; Smad4fl/fl palates. In Tgfbr2 mutant embryos, downregulation of Ctgf expression is associated with p38 mitogen-activated protein kinase (MAPK) overactivation, whereas loss of function of Smad4 itself leads to downregulation of Ctgf expression. We also found that CTGF regulates its own expression via TGF-β signaling. Osr2-Cre; Smad4fl/fl mice exhibit a defect in cell proliferation similar to that of Tgfbr2 mutant mice, as well as cleft palate. We detected no alteration in bone morphogenetic protein (BMP) downstream targets in Smad4 mutant palates, suggesting that the reduction in cell proliferation is due to defective transduction of TGF-β signaling via decreased Ctgf expression. Significantly, an exogenous source of CTGF was able to rescue the cell proliferation defect in both Tgfbr2 and Smad4 mutant palates. Collectively, our data suggest that CTGF regulates proliferation as a mediator of the canonical pathway of TGF-β signaling during palatogenesis.
机译：转化生长因子β（TGF-β）信号传导在颅面发育（包括pa骨形成）的调节中起关键作用。在这里，我们已经确定结缔组织生长因子（ Ctgf ）是成pa中TGF-β信号通路的下游目标。野生型胚胎中的 Ctgf 表达模式提示其可能参与味觉发育的关键过程。我们发现 Ctgf 表达在两个 Wnt1-Cre 中均被下调; Tgfbr2 fl / fl 和 Osr2-Cre ; Smad4 fl / fl 口感。在 Tgfbr2 突变胚胎中， Ctgf 表达的下调与p38丝裂原激活的蛋白激酶（MAPK）过度活化有关，而 Smad4 的功能丧失本身会导致 Ctgf 表达下调。我们还发现CTGF通过TGF-β信号传导调节其自身的表达。 Osr2-Cre ; Smad4 fl / fl 小鼠的细胞增殖缺陷与 Tgfbr2 突变小鼠相似，并且left裂。我们没有发现 Smad4 突变体上颚骨中骨形态发生蛋白（BMP）下游靶位的改变，这表明细胞增殖的减少是由于Tem-Ctgf降低导致的TGF-β信号转导缺陷所致。 em>表达式。重要的是，CTGF的外源来源能够挽救 Tgfbr2 和 Smad4 突变体上颚的细胞增殖缺陷。总体而言，我们的数据表明CTGF调节增殖，作为在成核过程中TGF-β信号传导经典途径的介质。

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