摘要
目的观察TERE1基因在正常小鼠腭发育和全反式视黄酸诱导的小鼠腭裂形成过程中的表达变化,探讨TERE1基因在腭裂发生中的作用。方法 ICR小鼠受孕后,将其随机分为实验组和对照组,各64只小鼠。于孕10 d(gestational day 10,GD10),经口灌胃一次给予实验组孕鼠80 mg/kg的全反式视黄酸、对照组孕鼠给予等体积的大豆油,并分别于GD11~GD18取两组胎鼠的腭板。于GD12取下小鼠胚胎腭移植体,以10-9~10-5 mol/L全反式视黄酸(all-trans retinoic acid,atRA)诱导,培养72 h后收获腭板。利用实时荧光定量PCR方法(quantitative real-time polymerasechain reaction,QRT-PCR)检测TERE1基因在正常腭组织和全反式视黄酸诱导的腭裂组织中的表达情况。结果 TERE1在正常、异常腭及培养腭板中均有表达。在GD11,异常腭中该基因的表达丰度高于正常腭,而在GD12~GD17,其表达丰度则低于正常腭(P<0.05)。10-9 mol/L atRA组和对照组的TERE1基因表达丰度差异无统计学意义(P>0.05),其他各atRA组该基因的表达丰度均低于对照组。结论在该试验条件下,atRA会抑制TERE1在腭中的表达,提示TERE1在腭的发生过程中可能起作用。
Objective To observe the expression of TERE1 gene in normal palates and all-trans retinoic acid-induced cleft palates during mouse embryogenesis,and explore the relation between TERE1 and the cleft palates.Methods At gestational day 10(GD10),the gestational mice of the treatment group were administered with 80 mg /kg atRA,and those of the control group were administered with the same volume soybean oil.The palates of all embryos were harvested during GD11-GD18.At GD12 Mouse embryonic palates were explanted and induced by atRA in different concentrations from 10-9 mol /L to 10^-5 mol /L and cultured for 72 h.The mRNA expression of TERE1 in all samples was measured by quantitative real-time polymerase chain reaction(QRT-PCR).Results TERE1 was expressed in all samples.At GD11 the mRNA expression of TERE1 in the cleft palate were higher than those in the normal palate,and at GD12-GD17,the expression of this gene in the cleft palates were lower than those in the normal palates.The mRNA expression of TERE1 in the 10^-9 mol /L atRA group had no difference incomparison with those of the negative control group,and the expressions of this gene in the other atRA groups were lower than those of the negative control group.Conclusion TERE1 maybe play a role during the development of palate and atRA probably affects the expression of TERE1 in palate.
出处
《毒理学杂志》
CAS
CSCD
北大核心
2010年第4期271-274,共4页
Journal of Toxicology
基金
浙江医药卫生项目(2008A126)
上海市公共卫生重点学科建设项目(08GZX0301)