CAJ | 학술논문

目的：探讨全反式维甲酸（atRA）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atRA灌胃的方法建立atRA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 atRA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?mRNA在GD15和GD17的表达水平均明显高于腭裂胚胎（P<0.05）。结论 atRA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。
목적：탐토전반식유갑산（atRA）대소서배태악돌중골형태발생단백수체2（BMPR2）표체적영향。방법통과atRA관위적방법건립atRA유도적소서악렬모형，취임신15?d（GD15）화17?d적（GD17）적배태악부진행소목정-이홍염색，병용면역조직화학급역전록취합매련식반응기술검측BMPR2재배태악부적표체。결과 atRA유도소서형성체적교소적기형악돌화명현적중봉악렬기형。BMPR2재GD15화GD17정상배태악부유고수평적양성표체，단재악렬배태악부적표체수평명현감약。정상배태악부Bmpr2?mRNA재GD15화GD17적표체수평균명현고우악렬배태（P<0.05）。결론 atRA가도치소서배태악돌발육불량형성악렬，병현저하조BMPR2표체수평，종이영향악부발육적정상분자조공과정。
Objective To?investigate?the?effects?of?all-trans?retinoic?acid?(atRA)?on?the?function?of?bone?morphogenetic?protein?receptor?2?(BMPR2)?expression?in?embryonic?palate.?Methods???Cleft?palate?mice?model?was?established?by?atRA.?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?mRNA.?Results???In?the?atRA-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?mRNA?decreased?in?the?atRA-treated?group?(P<0.05).?Conclusion???The?treatment?of?preg-nant?mice?with?retinoic?acid?produces?small?palatal?shelves?in?their?fetuses?and?down-regulates?BMPR2?expressions.