中文摘要：

目的 检测FMR1基因敲除小鼠海马组织中microRNA-125b（miR-125b）和miR-132表达水平,探讨脆性X智力低下蛋白（FMRP）缺失是否通过改变其转录后表达影响树突棘发育.方法 取FVB近交系雄性1周龄FMR1基因敲除型（K0）和同龄野生型（WT）小鼠各3只,取海马组织标本,应用microRNA芯片技术和荧光定量实时PCR检测miR-125b和miR-132的表达.结果 microRNA芯片检测显示,1周龄WT与KO小鼠海马组织miR-125b和miR-132的荧光值比较,差异无统计学意义（miR-125b：4 919.295±431.981比4 997.578±141.402;miR- 132：244.289±31.125比238.517±62.275,均P＞0.05）；荧光定量实时PCR检测显示,miR-125b和miR-132的相对表达量差异亦无统计学意义（miR-125b：11.45±0.32比11.55±0.43；miR- 132：18.28±0.34比18.50±0.40,均P＞0.05）.结论 脆性X综合征树突棘发育不良与miR-125b和miR-132的转录后表达水平无关.

英文摘要：

Objective To determine the expression ofmicroRNA-125b （miR-125b） and microRNA132 （miR-132） in hippocampus of FMR1 gene knockout mice,and to investigate whether fragile X mental retardation protein （FMRP） deletion interferes with expression of miR-125b and miR-132,and consequently with immature dendritic spine development.Methods The expression of miR-125b and miR-132 was detected in hippocampus harvested from 1-week-old FMR1 knockout male FVB inbred mice and age-matched wild-type mice （n=3 for each group） using microRNAs array detection and fluorescence quantitative real-time PCR.Results MicroRNAs array detection did not show any significant difference in fluorescence level between the two groups （miR-125b： 4 919.295±431.981 vs 4 997.578±141.402; miR-132：244.289±31.125 vs 238.517±62.275,both P〉0.05）.By fluorescence quantitative real-time PC R,the relative levels of miR-125b and miR-132 expression were statistically comparable between FMRl knockout mice and wild-type mice （miR-125b： 11.45±0.32 vs 11.55±0.43; miR -132：18.28 ± 0.34 vs 18.50±0.40,both P〉0.05）.Conclusion The immature dendritic spine development in fragile X syndrome is not associated with changes in post transcriptional expression levels of miR125b and miR-132.