Dauphinot Luce, Mockel Lionel, Cahu Julie, Jinnah H A, Ledroit Morgan, Potier Marie-Claude, Ceballos-Picot Irène
a CRICM, UPMC Hôpital de la Pitié-Salpêtrière , Paris , France.
Nucleosides Nucleotides Nucleic Acids. 2014;33(4-6):208-17. doi: 10.1080/15257770.2014.880477.
Lesch-Nyhan disease (LND) is an X-linked metabolic disease caused by various mutations in the gene HPRT1 encoding an enzyme of purine metabolism, hypoxanthine guanine phosphoribosyltransferase (HPRT). In its most severe form, LND patients suffer from overproduction of uric acid along with neurological or behavioural difficulties including self-injurious behaviours. To gain more insight into pathogenesis, we compared the transcriptome from human LND fibroblasts to normal human fibroblasts using a microarray with 60,000 probes corresponding to the entire human genome. Using stringent criteria, we identified 25 transcripts whose expression was significantly different between LND and control cells. These genes were confirmed by quantitative RT-PCR to be dysregulated in LND cells. Moreover, bioinformatic analysis of microarray data using gene ontology (GO) highlighted clusters of genes displaying biological processes most significantly affected in LND cells. These affected genes belonged to specific processes such as cell cycle and cell-division processes, metabolic and nucleic acid processes, demonstrating the specific nature of the changes and providing new insights into LND pathogenesis.
莱施-奈恩综合征(LND)是一种X连锁代谢疾病,由编码嘌呤代谢酶次黄嘌呤鸟嘌呤磷酸核糖转移酶(HPRT)的HPRT1基因中的各种突变引起。在最严重的形式下,LND患者会出现尿酸过度产生以及神经或行为困难,包括自我伤害行为。为了更深入了解发病机制,我们使用了一个包含对应整个人类基因组的60000个探针的微阵列,将人类LND成纤维细胞的转录组与正常人成纤维细胞进行了比较。使用严格的标准,我们鉴定出25个转录本,其在LND细胞和对照细胞之间的表达存在显著差异。这些基因通过定量RT-PCR得到证实,在LND细胞中表达失调。此外,使用基因本体论(GO)对微阵列数据进行的生物信息学分析突出了在LND细胞中受影响最显著的生物过程的基因簇。这些受影响的基因属于特定的过程,如细胞周期和细胞分裂过程、代谢和核酸过程,证明了变化的特异性,并为LND发病机制提供了新的见解。