Retinoic acid alters the proliferation and survival of the epithelium and mesenchyme and suppresses Wnt/β-catenin signaling in developing cleft palate.
Retinoic acid alters the proliferation and survival of the epithelium and mesenchyme and suppresses Wnt/β-catenin signaling in developing cleft palate.
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DOI：
10.1038/cddis.2013.424
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发表时间：
2013-10-31
影响因子：
9
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中科院分区：
文献类型：
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维甲酸（RA）有助于腭裂，然而，细胞和分子机制负责的有害影响发育腭尚不清楚。Wnt信号是腭裂的候选途径，并与RA在器官发育，因此，我们的目的是调查是否RA诱导腭裂也从改变Wnt信号。给小鼠注射RA分别通过调节控制细胞周期和p38 MAPK信号转导的分子来改变颅面组织中的细胞增殖和凋亡。这种由RA改变的细胞命运是导致腭裂100%发病率的关键机制。此外，在腭部发育的早期，维甲酸通过与维甲酸受体（RAR）的结合和激活，完全抑制了Wnt/β-catenin信号通路，从而导致了维甲酸诱导的腭裂。此外，PI 3 K/Akt信号通路也参与了RA的作用。我们的研究结果有助于阐明RA诱导腭裂的机制。
Retinoic acid (RA) contributes to cleft palate; however, the cellular and molecular mechanisms responsible for the deleterious effects on the developing palate are unclear. Wnt signaling is a candidate pathway in the cleft palate and is associated with RA in organ development; thus, we aim to investigate whether RA-induced cleft palate also results from altered Wnt signaling. Administration of RA to mice altered cell proliferation and apoptosis in craniofacial tissues by regulating molecules controlling cell cycle and p38 MAPK signaling, respectively. This altered cell fate by RA is a crucial mechanism contributing to 100% incidence of cleft palate. Moreover, Wnt/β-catenin signaling was completely inhibited by RA in the early developing palate via its binding and activation with RA receptor (RAR) and is responsible for RA-induced cleft palate. Furthermore, PI3K/Akt signaling was also involved in actions of RA. Our findings help in elucidating the mechanisms of RA-induced cleft palate.
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