摘要
目的:丙戊酸(valproic acid,VPA)可导致组蛋白乙酰化/去乙酰化失衡,一过性干扰孕鼠子宫内胚胎发育,诱导胎鼠心脏发育畸形,造成小鼠先天性心脏畸形。本实验探讨组蛋白乙酰化/去乙酰化一过性失衡的"开关机制"在先天性心脏畸形中的作用。方法VPA作用后,应用RT PCR和Western blot检测全胚胎HDAC1与HDAC2基因和蛋白的相对表达量。结果:VPA作用后全胚胎的HDAC1与HDAC2基因和蛋白的相对表达量均明显下调。结论:组蛋白乙酰化/去乙酰化失衡与先天心脏发育畸形密切相关。
Objective：To explore the role of histone acetylation/deacetylation imbalance in the pathogenesis of congenital heart disease. Methods Using VPA to interfere with the development of mttrine intrauterine embryos at specific time points and develop an embryonic murine cardiac abnormalities model. The mRNA and protein expressions of HDAC1 and HDAC2 were assessed by RT - PCR and Westemblot. Results The expression of HDAC1 and HDAC2 gene/protein both decreased significantly in the whole murine embryo after VPA treatment by RT- PCR and Western blot detection. Conclusion The histone acetylatian/deacetylation imbalance may be involved in the pathogenesis of congenital heart diseases.
出处
《激光杂志》
CAS
CSCD
北大核心
2013年第4期91-92,共2页
Laser Journal
基金
国家自然科学基金面上项目资助
编号:81270226
四川省科技厅2013年科技支撑项目资助
关键词
组蛋白乙酰化
去乙酰化失衡
先天性心脏病
发病机制
histone acetylation/deaeetylation imbalance
congenital heartdisease
pathogenesis
