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Generation of Organoids from Mouse Extrahepatic Bile Ducts
Published on: April 23, 2019
Gene expression profiling of extrahepatic ducts in children with biliary atresia
Jiang Wang1, Wei Wang1, Rui Dong1
1Department of Pediatric Surgery, Children's Hospital of Fudan University and The Key Laboratory of Neonatal Disease, Chinese Ministry of Health Shanghai, China.
Insights
Biliary atresia (BA) is a neonatal inflammatory condition affecting bile ducts. Gene expression profiling identified 140 differentially expressed genes, with IL7, CLDN2, and VCAM1 potentially involved in BA pathogenesis and fibrosis.
Area of Science:
- Neonatal immunology
- Gastroenterology
- Molecular biology
Background:
- Biliary atresia (BA) is a serious neonatal inflammatory bile duct disease with unknown causes.
- It affects both intrahepatic and extrahepatic bile ducts, leading to liver damage.
Purpose of the Study:
- To identify novel molecular targets for biliary atresia (BA) research.
- To investigate gene expression profiles in extrahepatic bile duct tissues of BA infants.
Main Methods:
- Gene expression profiling using Affymetrix human microarray on porta hepatis and common bile duct tissues.
- Quantitative RT-PCR (qRT-PCR) for result validation.
- Gene Ontology (GO) and pathway analyses for functional insights.
Main Results:
- 140 differentially expressed genes identified: 19 up-regulated, 121 down-regulated.
- GO analysis suggests involvement of cell adhesion, extracellular matrix, and protein digestion in porta hepatis fibrosis.
- IL7 and CLDN2 were significantly up-regulated; VCAM1 expression correlated with liver fibrosis severity.
Conclusions:
- Aberrant gene expression in porta hepatis is linked to fibrosis in biliary atresia (BA).
- IL7, CLDN2, and VCAM1 are potential key players in BA etiology and progression.
- Further research into these genes may elucidate BA's pathological mechanisms.
Abstract:
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.
