维甲酸诱导腭裂发生的过程中对TGF-β/Smad信号途径的抑制作用  

Inhibition of TGF-β/Smad Pathway is Implicated in Cleft Palate Induced by All-trans Retinoic Acid

作　　者：刘小转[1] 潘新娟[1] 张丽[1] 

机构地区：[1]河南科技大学医学院,河南洛阳471003

出　　处：《河南科技大学学报（医学版）》2013年第1期1-4,共4页Journal of Henan University of Science & Technology:Medical Science

摘　　要：目的探讨维甲酸在诱导腭裂发生过程中对Smad2磷酸化的影响,并分析其可能的致畸机制。方法建立维甲酸诱导的腭裂模型,利用HE染色观察维甲酸诱导腭裂发生的过程;应用免疫组化检测E12 d、E13 d、E14.5 d、E15 d、E15.5 d、E16 d(Ed:Embryonic day)对照组和实验组胎鼠模型腭突中嵴上皮内P-Smad2蛋白的表达。结果在腭突融合过程中,内源性的Smad2通过磷酸化能够被激活。与对照组相比,维甲酸可抑制腭突中嵴上皮中Smad2的磷酸化表达。结论维甲酸诱导腭裂的发生,与中嵴上皮细胞中Smad2磷酸化的抑制密切相关。Objective To investigate the effect of all-trans retinoic acid （atRA） on phosphorylation of Smad during palatogenesis and the underlying mechanisms of teratogenesis. Methods To establish animal model of RA-induced cleft palate （CP）. We detected the expression of P-Smad in medial edge epithelial （MEE） of El3 d, E14.5 d, E15 d, E15.5 d and E16 d （Ed： Embryonic day） in control group and RA treated group by using immunohistochemistry. Results Smad2 were endogenously activated during the fusion process. In contrast, atRA treatment decreased phosphorylation of Smad2 in MEE. Conclusion RA might lead to CP through inhibition of phosphoraylation of Smad2 in MEE.

关 键 词：腭裂 动物模型 全反式维甲酸 中嵴上皮 SMAD2 

分 类 号：R782.22[医药卫生—口腔医学]