Dexamethasone alters epithelium proliferation and survival and suppresses Wnt/β-catenin signaling in developing cleft palate
Dexamethasone alters epithelium proliferation and survival and suppresses Wnt/β-catenin signaling in developing cleft palate
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DOI：
10.1016/j.fct.2013.02.003
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发表时间：
2013-06-01
影响因子：
4.3
通讯作者：
Lu, Feng
中科院分区：
文献类型：
--
作者：
Hu, Xiao;Gao, Jian Hua;Lu, Feng
地塞米松（Dex）有助于腭裂，但细胞和分子机制负责对发育中的腭裂的有害影响尚不清楚。Wnt信号通路是dex诱导骨质疏松的病因机制，因此本研究旨在确定dex诱导的腭裂是否由Wnt信号通路改变引起。右美托咪定完全抑制小鼠典型Wnt/ β -连环蛋白信号通路，改变发育胚胎颅面上皮细胞增殖和凋亡。因此，下调Wnt/ β -连环蛋白信号与dex诱导的腭裂有关。此外，导致腭裂的细胞命运改变，延迟腭架上升和腭不融合是腭裂的重要机制。我们的发现有助于阐明dex诱发腭裂的机制。(C) 2013 Elsevier Ltd.版权所有。
Dexamethasone (Dex) contributes to a cleft palate, but the cellular and molecular mechanisms responsible for the deleterious effect on the developing palate are unclear. Wnt signaling is a causal mechanism of Dex-induced osteoporosis, so this study was conducted to determine whether Dex-induced cleft palate may result from altered Wnt signaling. Administration of Dex to mice completely inhibited canonical Wnt/beta-catenin signaling and altered cell proliferation and apoptosis of the craniofacial epithelium in developing embryos. Thus, downregulated Wnt/beta-catenin signaling was associated with Dex-induced cleft palate. Moreover, altered cell fate by Dex responsible for small palates, delaying shelf elevation and unfused palates was a crucial mechanism in cleft palate. Our findings help in elucidating the mechanisms of Dex-induced cleft palate. (C) 2013 Elsevier Ltd. All rights reserved.