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首页> 外文期刊>Cell death & disease. >Transferrin receptor facilitates TGF-β and BMP signaling activation to control craniofacial morphogenesis
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Transferrin receptor facilitates TGF-β and BMP signaling activation to control craniofacial morphogenesis

机译：转铁蛋白受体促进TGF- β和BMP信号激活，以控制颅面形态发生

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摘要

The Pierre Robin Sequence (PRS), consisting of cleft palate, glossoptosis and micrognathia, is a common human birth defect. However, how this abnormality occurs remains largely unknown. Here we report that neural crest cell (NCC)-specific knockout of transferrin receptor (Tfrc), a well known transferrin transporter protein, caused micrognathia, cleft palate, severe respiratory distress and inability to suckle in mice, which highly resemble human PRS. Histological and anatomical analysis revealed that the cleft palate is due to the failure of palatal shelves elevation that resulted from a retarded extension of Meckel’s cartilage. Interestingly, Tfrc deletion dramatically suppressed both transforming growth factor- β (TGF- β ) and bone morphogenetic protein (BMP) signaling in cranial NCCs-derived mandibular tissues, suggesting that Tfrc may act as a facilitator of these two signaling pathways during craniofacial morphogenesis. Together, our study uncovers an unknown function of Tfrc in craniofacial development and provides novel insight into the etiology of PRS.
机译：皮埃尔·罗宾序列（PRS）由left裂，舌突和微棘突症组成，是人类常见的出生缺陷。然而，这种异常如何发生仍然是未知的。在这里，我们报告神经传递细胞受体（Tfrc）的神经c细胞（NCC）特异性敲除，一种众所周知的转铁蛋白转运蛋白，引起小白点症，c裂，严重的呼吸窘迫和无法吮吸小鼠，这与人PRS非常相似。组织学和解剖学分析表明，left裂是由于Meckel软骨延缓发育而导致的shelves架抬高失败。有趣的是，Tfrc缺失显着抑制了颅NCCs衍生的下颌组织中的转化生长因子β（TGF-β）和骨形态发生蛋白（BMP）信号传导，这表明Tfrc可能在颅面形态发生过程中充当了这两个信号通路的促进剂。总之，我们的研究揭示了Tfrc在颅面发育中的未知功能，并为PRS的病因学提供了新颖的见解。

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