Wnt2 signaling is necessary and sufficient to activate the airway smooth muscle program in the lung by regulating myocardin/Mrtf-B and Fgf10 expression.
Wnt2 signaling is necessary and sufficient to activate the airway smooth muscle program in the lung by regulating myocardin/Mrtf-B and Fgf10 expression.
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DOI：
10.1016/j.ydbio.2011.06.011
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发表时间：
2011-08-15
影响因子：
2.7
通讯作者：
Morrisey EE
中科院分区：
文献类型：
--
作者：
Goss AM;Tian Y;Cheng L;Yang J;Zhou D;Cohen ED;Morrisey EE
肺中的平滑肌被认为来源于发育中的肺间充质。平滑肌的形成依赖于出芽上皮和相邻间充质之间的自分泌和旁分泌信号的协调来控制其增殖和分化。然而，启动肺平滑肌特化和分化的最早方面的途径知之甚少。在这里，我们确定Wnt 2配体作为肺气道平滑肌发育的最早方面的关键调节剂。使用Wnt 2损失和增益的功能模型，我们表明，Wnt 2信号是必要的和足够的激活的转录和信号网络的平滑肌规范和分化，包括心肌蛋白/Mrtf-B和信号因子FGF 10的关键。这些研究将Wnt 2置于促进肺气道平滑肌发育的最早方面的信号分子的层次中。
Smooth muscle in the lung is thought to derive from the developing lung mesenchyme. Smooth muscle formation relies upon coordination of both autocrine and paracrine signaling between the budding epithelium and adjacent mesenchyme to govern its proliferation and differentiation. However, the pathways initiating the earliest aspects of smooth muscle specification and differentiation in the lung are poorly understood. Here, we identify the Wnt2 ligand as a critical regulator of the earliest aspects of lung airway smooth muscle development. Using Wnt2 loss and gain of function models, we show that Wnt2 signaling is necessary and sufficient for activation of a transcriptional and signaling network critical for smooth muscle specification and differentiation including myocardin/Mrtf-B and the signaling factor Fgf10. These studies place Wnt2 high in a hierarchy of signaling molecules that promote the earliest aspects of lung airway smooth muscle development.
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影响因子：
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作者：
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通讯作者：
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