Lee I J, Soh Y, Song B J
Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20852, USA.
Biochem Biophys Res Commun. 1997 Nov 17;240(2):309-13. doi: 10.1006/bbrc.1997.7655.
The molecular pathogenesis of fetal alcohol syndrome (FAS) has not been well elucidated. The technique of mRNA differential display was used to characterize the etiology and to identify potential markers for FAS. Out of approximately 1,080 mRNA transcripts in mouse embryos that were analyzed, the levels of three mRNAs were altered by ethanol. Two of these mRNAs (one novel and one encoding heat shock protein 47) were also modulated by another teratogen, 3-methylcholanthrene. The third mRNA, encoding alpha-tropomyosin, was specifically up-regulated by ethanol. Consistent with the Northern blot data, immunoblot analysis demonstrated that the level of alpha-tropomyosin protein (31 kDa, most likely a brain specific isoform) was elevated in the embryos exposed to ethanol.
胎儿酒精综合征(FAS)的分子发病机制尚未完全阐明。采用mRNA差异显示技术来表征其病因并鉴定FAS的潜在标志物。在分析的小鼠胚胎中约1080种mRNA转录本中,有三种mRNA的水平受到乙醇的影响而改变。其中两种mRNA(一种是新的,另一种编码热休克蛋白47)也受到另一种致畸剂3-甲基胆蒽的调节。第三种编码α-原肌球蛋白的mRNA则被乙醇特异性上调。与Northern印迹数据一致,免疫印迹分析表明,暴露于乙醇的胚胎中α-原肌球蛋白蛋白(31 kDa,很可能是一种脑特异性同工型)的水平升高。