Wang Jiang, Wang Wei, Dong Rui, Zhao Rui, Jin Zhu, Shen Wenjun, Zheng Shan
Department of Pediatric Surgery, Children's Hospital of Fudan University and The Key Laboratory of Neonatal Disease, Chinese Ministry of Health Shanghai, China.
Int J Clin Exp Med. 2015 Apr 15;8(4):5186-96. eCollection 2015.
As an inflammatory obliterative cholangiopathy of neonates, biliary atresia (BA) affects both intrahepatic and extrahepatic bile ducts. Its etiology has remained largely unknown. Gene expression profiling was conduced for extrahepatic bile duct tissues (including porta hepatis & common bile duct) to identify novel targets for further studies of BA. Among these tissues, porta hepatis was regarded as fibrosis group while common bile duct as self-control group. The analysis of gene expression profile in these tissues was performed with Affymetrix human microarray. Quantitative RT-PCR (qRT-PCR) was performed to confirm these results. The differential expressions of genes were identified through fold-change filtering. Gene Ontology (GO) and pathway analyses were performed using standard enrichment computation method. It was found that a total of 140 genes were differentially expressed between porta hepatis and common bile duct tissues, 19 genes up-regulated and 121 genes down-regulated. Moreover, GO analysis found that cell adhesion molecules, extracellular matrix formation, protein digestion & absorption functions may be involved in the pathogenesis of porta hepatis fibrosis. Lastly the qRT-PCR data confirmed that IL7 and CLDN2 were significantly up-regulated and both might be involved in the etiology of BA, the expression level of VCAM1 was positively correlated with severity of liver fibrosis in the BA infants. Our results demonstrated that the expressions of these aberrant genes responding to fibrosis in porta hepatis of patients with BA. Further studies of these genes may provide useful insights into the pathological mechanisms of BA.
作为一种新生儿炎症性闭塞性胆管病,胆道闭锁(BA)会影响肝内和肝外胆管。其病因在很大程度上仍然未知。对肝外胆管组织(包括肝门和胆总管)进行基因表达谱分析,以确定用于BA进一步研究的新靶点。在这些组织中,肝门被视为纤维化组,而胆总管作为自身对照组。使用Affymetrix人类微阵列对这些组织中的基因表达谱进行分析。进行定量逆转录聚合酶链反应(qRT-PCR)以证实这些结果。通过倍数变化筛选鉴定基因的差异表达。使用标准富集计算方法进行基因本体论(GO)和通路分析。结果发现,肝门和胆总管组织之间共有140个基因差异表达,19个基因上调,121个基因下调。此外,GO分析发现细胞粘附分子、细胞外基质形成、蛋白质消化和吸收功能可能参与肝门纤维化的发病机制。最后,qRT-PCR数据证实IL7和CLDN2显著上调,两者可能都参与BA的病因,VCAM1的表达水平与BA婴儿肝纤维化的严重程度呈正相关。我们的结果表明,这些异常基因在BA患者肝门中对纤维化有反应。对这些基因的进一步研究可能为BA的病理机制提供有用的见解。