Ontology highlight
ABSTRACT:
PROVIDER: PRJNA890380 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21915843_1.fastq.gz | Fastqsanger.gz | |||
| SRR21915843_2.fastq.gz | Fastqsanger.gz | |||
| SRR21915844_1.fastq.gz | Fastqsanger.gz | |||
| SRR21915844_2.fastq.gz | Fastqsanger.gz | |||
| SRR21915845_1.fastq.gz | Fastqsanger.gz |
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Project description:Clonorchiasis is associated with bile duct malignancy and the subsequent development of cholangiocarcinoma. Although this is likely caused by adult Clonorchis sinensis and its excretory-secretory products (ESP), the precise molecular mechanisms remain obscure. To evaluate the effect of C. sinensis infection on differential gene expression in host hepatocytes, we used cDNA microarrays in human cholangiocarcinoma cells through the mimicking of C. sinensis infestation, and analyzed differential mRNA expression patterns of host cells. Keywords: Time course
2008-07-24 | GSE12213 | GEO
Project description:We examined gene expression profiles (27028 genes) in the livers of Sprague-Dawley rats with no infection and at 2 and 4 weeks after Clonorchis sinensis infection using Whole Rat Genome Microarray 4x44K v3 (GPL14745, Agilent-028282)
2019-08-29 | GSE136575 | 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: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.
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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.
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Project description:We investigated bile-acid induced gene expression patterns in regulatory T-cells, and applied those gene sets to gene expression profiles of liver samples obtained from children with biliary atresia and intrahepatic cholestasis. Patient subgroups identified using the regulatory T-cell gene sets were then assessed for association with two-year outcome in patients with biliary atresia.
2022-12-20 | GSE221346 | GEO
Project description:Analysis of host response to the infected Clonorchis sinensis metacercariae and adult worm. The infected tissues evidenced altered expression of genes involved in systems such as immune response and cell cycle regulation, as compared with normal tissues. Total RNA obtained from isolated liver tissues subjected to 1, 2, 4, and 6 weeks post-infection compared to uninfected liver tissues.
2010-05-20 | E-GEOD-15447 | biostudies-arrayexpress
Project description:Clonorchis sinensis is a zoonotic parasite causing clonorchiasis associated with human diseases such as biliary calculi, cholecystitis, liver cirrhosis, and is classified as carcinogenic to humans for cholangiocarcinoma. MicroRNAs (miRNAs) are non-coding, regulating small RNA molecules essential for the complex life cycle of parasites and involved in parasitic infections. To identify and characterize miRNAs expressed in adult C. sinensis residing chronically in the biliary tract, we developed an integrative approach combining deep sequencing, bioinformatic predictions with stem-loop real-time PCR analysis. Here we report the use of this approach to identify and clone 6 new and 62,512 conserved C. sinensis miRNAs which belong to 284 families. There is strong bias on families, family members and sequence nucleotides in C. sinensis. Uracil is the dominant nucleotide, particularly at positions 1, 14 and 22, which were located approximately at the beginning, middle and the end of conserved miRNAs. There is no significant M-bM-^@M-^\seed regionM-bM-^@M-^] at the first and ninth positions commonly found in human, animals and plants. Categorization of conserved miRNAs indicated that miRNAs of C. sinensis are still innovated and concentrated along three branches of the phylogenetic tree leading to bilaterians, insects and coelomates. There are two miRNA strategies in C. sinensis for its parasitic life: keeping a large category of miRNA families of different animals and keeping a stringent conserved seed region with high active innovation in other place of miRNA mainly in the middle and the end, which are perfect for the parasite to perform its complex life style and for host changes. The present study represents the first large scale characterization of C. sinensis miRNAs, which have implications for understanding the complex biology of this zoonotic parasite, as well as the miRNA studies of other related species such as Opisthorchis felineus and O. viverrini of human and animal health significance. Analysis of miRNA profile in parasite of C. sinensis
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Project description:Clonorchis sinensis (Cs) infection is prevalent in Southeast Asia and has been classified as a Group I carcinogen by the International Agency for Research on Cancer, posing significant risks to the human liver and biliary system. While recent studies have linked Cs infection to poorer outcomes in hepatocellular carcinoma (HCC) patients, the precise molecular mechanisms underlying its effect on HCC remain to be fully elucidated. This study investigates the epigenetic changes in Cs-infected HCC using whole-genome bisulfite sequencing and whole-genome oxidative bisulfite sequencing to map 5-methylcytosine and 5-hydroxymethylcytosine profiles at single-nucleotide resolution. We identified 29 differentially methylated regions and 13 differentially hydroxymethylated regions in Cs-infected HCC, which were associated with 28 differentially methylated/hydroxymethylated-associated genes (DAGs/DhAGs). The methylation levels of four promoter Cytosine-phosphate-Guanine (CpG) sites of DAGs/DhAGs were found to correlate with prognosis in Cs-infected HCC, while two key DMR/DhMR-associated genes, DHDH and KCNQ3, were significantly linked to overall survival of HCC. Our study provides the first detailed epigenetic map of Cs-associated HCC, uncovering novel insights into potential biomarkers and therapeutic targets that could enhance prognostic predictions and inform treatment strategies for patients affected by this condition.
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