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骨形态发生蛋白受体2在维甲酸诱导腭裂小鼠胚胎腭突中的表达 被引量:4

Expression of bone morphogenetic protein receptor 2 in cleft mouse embryonic palate induced by retinoic acid
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摘要 目的探讨全反式维甲酸(at RA)对小鼠胚胎腭突中骨形态发生蛋白受体2(BMPR2)表达的影响。方法通过at RA灌胃的方法建立at RA诱导的小鼠腭裂模型,取妊娠15 d(GD15)和17 d的(GD17)的胚胎腭部进行苏木精-伊红染色,并用免疫组织化学及逆转录聚合酶链式反应技术检测BMPR2在胚胎腭部的表达。结果 at RA诱导小鼠形成体积较小的畸形腭突和明显的中缝腭裂畸形。BMPR2在GD15和GD17正常胚胎腭部有高水平的阳性表达,但在腭裂胚胎腭部的表达水平明显减弱。正常胚胎腭部Bmpr2 m RNA在GD15和GD17的表达水平均明显高于腭裂胚胎(P<0.05)。结论 at RA可导致小鼠胚胎腭突发育不良形成腭裂,并显著下调BMPR2表达水平,从而影响腭部发育的正常分子调控过程。 Objective To investigate the effects of all-trans retinoic acid(at RA) on the function of bone morphogenetic protein receptor 2(BMPR2) expression in embryonic palate. Methods Cleft palate mice model was established by at RA. On gestation day(GD) 15 and GD17, the pregnant mice were killed to obtain the embryos from the uteri. The embryonic palates were stained with hematoxylin-eosin, and the remaining sections were used for the immunohistochemistry of BMPR2 detection. Reverse transcription-polymerase chain reaction was performed to detect the expression levels of Bmpr2 m RNA. Results In the at RA-treated group, short extensions and failure to fuse with each other were observed. The positive expression of BMPR2 was detected in developing palatal process from GD 15 to GD 17 in the control group. Compared with those of the control group, BMPR2 protein and Bmpr2 m RNA decreased in the at RA-treated group(P0.05). Conclusion The treatment of pregnant mice with retinoic acid produces small palatal shelves in their fetuses and down-regulates BMPR2 expressions.
出处 《华西口腔医学杂志》 CAS CSCD 北大核心 2015年第4期377-382,共6页 West China Journal of Stomatology
基金 国家自然科学基金资助项目(81300862) 深圳市医疗卫生类科研基金资助项目(201302202) 深圳市南山区卫生科技基金资助项目(2012040)
关键词 骨形态发生蛋白受体2 维甲酸 腭裂 bone morphogenetic protein receptor 2 retinoic acid cleft palate
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