Nodale Cristina, Ceccarelli Simona, Giuliano Mariateresa, Cammarota Marcella, D'Amici Sirio, Vescarelli Enrica, Maffucci Diana, Bellati Filippo, Panici Pierluigi Benedetti, Romano Ferdinando, Angeloni Antonio, Marchese Cinzia
Department of Experimental Medicine, Sapienza University of Rome, Rome, Italy.
Department of Experimental Medicine, Biotechnology and Molecular Biology Section, Second University of Naples, Naples, Italy.
PLoS One. 2014 Mar 7;9(3):e91010. doi: 10.1371/journal.pone.0091010. eCollection 2014.
Mayer-Rokitansky-Küster-Hauser syndrome (MRKHS) is a rare disease characterized by congenital aplasia of uterus and vagina. Although many studies have investigated several candidate genes, up to now none of them seem to be responsible for the aetiology of the syndrome. In our study, we identified differences in gene expression profile of in vitro cultured vaginal tissue of MRHKS patients using whole-genome microarray analysis. A group of eight out of sixteen MRKHS patients that underwent reconstruction of neovagina with an autologous in vitro cultured vaginal tissue were subjected to microarray analysis and compared with five healthy controls. Results obtained by array were confirmed by qRT-PCR and further extended to other eight MRKHS patients. Gene profiling of MRKHS patients delineated 275 differentially expressed genes, of which 133 downregulated and 142 upregulated. We selected six deregulated genes (MUC1, HOXC8, HOXB2, HOXB5, JAG1 and DLL1) on the basis of their fold change, their differential expression in most patients and their relevant role in embryological development. All patients showed upregulation of MUC1, while HOXB2 and HOXB5 were downregulated, as well as Notch ligands JAG1 and DLL1 in the majority of them. Interestingly, HOXC8 was significantly upregulated in 47% of patients, with a differential expression only in MRKHS type I patients. Taken together, our results highlighted the dysregulation of developmental genes, thus suggesting a potential alteration of networks involved in the formation of the female reproductive tract and providing a useful clue for understanding the pathophysiology of MRKHS.
迈耶-罗基坦斯基-库斯特-豪泽综合征(MRKHS)是一种罕见疾病,其特征为先天性子宫和阴道发育不全。尽管许多研究已经对多个候选基因进行了调查,但到目前为止,似乎没有一个基因与该综合征的病因有关。在我们的研究中,我们使用全基因组微阵列分析,确定了MRHKS患者体外培养的阴道组织基因表达谱的差异。16名接受自体体外培养阴道组织进行新阴道重建的MRKHS患者中的8名被纳入微阵列分析,并与5名健康对照进行比较。通过阵列获得的结果通过qRT-PCR得到证实,并进一步扩展到其他8名MRKHS患者。MRKHS患者的基因谱显示有275个差异表达基因,其中133个下调,142个上调。我们根据它们的倍数变化、在大多数患者中的差异表达以及它们在胚胎发育中的相关作用,选择了6个失调基因(MUC1、HOXC8、HOXB2、HOXB5、JAG1和DLL1)。所有患者均显示MUC1上调,而HOXB2和HOXB5下调,大多数患者中Notch配体JAG1和DLL1也下调。有趣的是,47%的患者中HOXC8显著上调,且仅在I型MRKHS患者中有差异表达。综上所述,我们的结果突出了发育基因的失调,从而提示参与女性生殖道形成的网络可能发生改变,并为理解MRKHS的病理生理学提供了有用线索。