Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1121599 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29346726_1.fastq.gz | Fastqsanger.gz | |||
| SRR29346726_2.fastq.gz | Fastqsanger.gz | |||
| SRR29346727_1.fastq.gz | Fastqsanger.gz | |||
| SRR29346727_2.fastq.gz | Fastqsanger.gz | |||
| SRR29346728_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 112 |
Similar Datasets
Project description:Biliary obstruction and cholangiocyte hyperproliferation are important features of cholangiopathies affecting the large extrahepatic bile ducts (EHBD). The mechanisms underlying obstruction-induced cholangiocyte proliferation in the EHBD remain poorly understood. Developmental pathways, such as WNT signaling, have been implicated in regulating injury responses in many tissues, including the liver and bile ducts. To investigate the contribution of WNT signaling to the EHBD cholangiocyte proliferative response to obstructive injury, we conducted a comprehensive study using complementary in vivo and in vitro models with pharmacologic interventions and computational approaches. To model obstruction, we used bile duct ligation (BDL) in mice. Human and mouse biliary organoids and mouse biliary explants were used to investigate the effects of WNT activation and inhibition in vitro. We observed a rapid upregulation of WNT ligand expression associated with increased biliary proliferation following obstruction. Cholangiocytes were identified as both WNT ligand-expressing cells and WNT responsive cells. Inhibition of WNT signaling decreased cholangiocyte proliferation in vivo and in vitro, while activation increased proliferation. WNT proliferative effects on cholangiocytes were β-catenin-dependent. Our studies suggest that cholangiocyte-derived WNT ligands can activate canonical WNT signaling to induce proliferation after obstructive injury. These findings implicate the WNT pathway in injury-induced cholangiocyte proliferation within the EHBD.
2025-02-12 | GSE280724 | GEO
Project description:Biliary obstruction and cholangiocyte hyperproliferation are important features of cholangiopathies affecting the large extrahepatic bile ducts (EHBD). The mechanisms underlying obstruction-induced cholangiocyte proliferation in the EHBD remain poorly understood. Developmental pathways, such as WNT signaling, have been implicated in regulating injury responses in many tissues, including the liver and bile ducts. To investigate the contribution of WNT signaling to the EHBD cholangiocyte proliferative response to obstructive injury, we conducted a comprehensive study using complementary in vivo and in vitro models with pharmacologic interventions and computational approaches. To model obstruction, we used bile duct ligation (BDL) in mice. Human and mouse biliary organoids and mouse biliary explants were used to investigate the effects of WNT activation and inhibition in vitro. We observed a rapid upregulation of WNT ligand expression associated with increased biliary proliferation following obstruction. Cholangiocytes were identified as both WNT ligand-expressing cells and WNT responsive cells. Inhibition of WNT signaling decreased cholangiocyte proliferation in vivo and in vitro, while activation increased proliferation. WNT proliferative effects on cholangiocytes were β-catenin-dependent. Our studies suggest that cholangiocyte-derived WNT ligands can activate canonical WNT signaling to induce proliferation after obstructive injury. These findings implicate the WNT pathway in injury-induced cholangiocyte proliferation within the EHBD.
2025-02-12 | GSE280691 | GEO
Project description:Biliary obstruction and cholangiocyte hyperproliferation are important features of cholangiopathies affecting the large extrahepatic bile duct (EHBD). The mechanisms underlying obstruction-induced cholangiocyte proliferation in the EHBD remain poorly understood. Developmental pathways, such as WNT signaling, have been implicated in regulating injury responses in many tissues, including the liver and bile ducts. To investigate the contribution of WNT signaling to the EHBD cholangiocyte proliferative response to obstructive injury, we conducted a comprehensive study using complementary in vivo and in vitro models with pharmacologic interventions and computational approaches. To model obstruction, we used bile duct ligation (BDL) in mice. Human and mouse biliary organoids and mouse biliary explants were used to investigate the effects of WNT activation and inhibition in vitro. We observed a rapid upregulation of WNT ligand expression associated with increased biliary proliferation following obstruction. Cholangiocytes were identified as both WNT ligand-expressing cells and WNT responsive cells. Inhibition of WNT signaling decreased cholangiocyte proliferation in vivo and in vitro, while activation increased proliferation. WNT proliferative effects on cholangiocytes were β-catenin-dependent. Our studies suggest that cholangiocyte-derived WNT ligands can activate canonical WNT signaling to induce proliferation after obstructive injury. These findings implicate the WNT pathway in injury-induced cholangiocyte proliferation within the EHBD.
2025-02-12 | GSE280889 | GEO
Project description:Identification of differential gene expression uging endoscopic biliary brushings Bile duct brishings of benign biliary strictures and malignant biliary strictures, samples snap frozen in liquid nitrogen
2012-03-01 | E-GEOD-34166 | biostudies-arrayexpress
Project description:mRNA expression profiling of ERCP biliary brushings of malignant biliary strictures
| PRJNA149713 | ENA
Project description:We have completed the Arraystar Human circRNA Array V2 analysis of 10 bile exosome samples (5 cholangiocarcinoma-induced biliary obstruction vs. 5 benign biliary obstruction). Total RNA from each sample was quantified using the NanoDrop ND-1000. The sample preparation and microarray hybridization were performed based on the Arraystar’s standard protocols. Briefly, total RNAs were digested with Rnase R (Epicentre, Inc.) to remove linear RNAs and enrich circular RNAs. Then, the enriched circular RNAs were amplified and transcribed into fluorescent cRNA utilizing a random priming method (Arraystar Super RNA Labeling Kit; Arraystar). The labeled cRNAs were hybridized onto the Arraystar Human circRNA Array V2 (8x15K, Arraystar). After having washed the slides, the arrays were scanned by the Agilent Scanner G2505C. Agilent Feature Extraction software (version 11.0.1.1) was used to analyze acquired array images. Quantile normalization and subsequent data processing were performed using the R software limma package. Differentially expressed circRNAs with statistical significance between two groups were identified through Volcano Plot filtering. Differentially expressed circRNAs between two samples were identified through Fold Change filtering. Hierarchical Clustering was performed to show the distinguishable circRNAs expression pattern among samples.
2024-04-20 | GSE228477 | GEO