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目的探究NCAM1在人类神经管畸形胚胎中的作用机制。方法提取NTDs组以及同周对照组胚胎脑组织,应用人类基因组U133Plus2.0芯片杂交,比较得出差异表达谱。所有差异表达基因按照功能分类。检测目的基因NCAM1的差异表达,并应用半定量RT-PCR方法以及免疫组化验证其mRNA及蛋白的改变。结果芯片显示出NTDs较正常对照组基因谱有较大的差异改变,总共检测到22209条基因的改变,其中2倍以上增高表达的74条,2倍以上降低表达的387条,分属于物质代谢、基因表达调控、信号转导、凋亡等途径。NCAM1呈21.8倍高表达。RT-PCR以及免疫组化也验证其mRNA及蛋白呈现高表达结果(P<0.01)。结论人类神经管畸形是不同阶段发展的复杂事件,作为细胞表面粘附分子的NCAM1在神经管畸形的发生发展过程中起了重要的作用。
Objective To explore the mechanism of NCAM1 in human neural tube defects embryos. Methods The embryonic brain tissues of NTDs group and the same week control group were extracted and compared with human U133Plus2.0. The differential expression profiles were obtained. All differentially expressed genes are classified by function. The differential expression of the target gene NCAM1 was detected and the mRNA and protein changes were verified by semi-quantitative RT-PCR and immunohistochemistry. Results The results showed that the NTDs were significantly different from those in the normal control group. A total of 22,209 gene changes were detected, of which 74 were up-regulated more than 2-fold and 387 down-regulated more than 2-fold, , Regulation of gene expression, signal transduction, apoptosis and other pathways. NCAM1 was 21.8 fold higher expression. RT-PCR and immunohistochemistry also confirmed the high expression of mRNA and protein (P <0.01). Conclusions Human neural tube defects are complex events in different stages of development. NCAM1, a cell surface adhesion molecule, plays an important role in the development of neural tube defects.