Ontology highlight
ABSTRACT:
PROVIDER: PRJNA827104 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18791516.fastq.gz | Fastqsanger.gz | |||
| SRR18791517.fastq.gz | Fastqsanger.gz | |||
| SRR18791518.fastq.gz | Fastqsanger.gz | |||
| SRR18791519.fastq.gz | Fastqsanger.gz | |||
| SRR18791520.fastq.gz | Fastqsanger.gz |
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Project description:The aim is to characterize rat liver fibrosis induced by bile duct ligation (BDL). To induce hepatic fibrosis, Male Sprague Dawley rats (9-12 weeks of age and 380-420 g of weight upon arrival, supplied by Beijing Vital River laboratory animal Co., Ltd.) underwent surgery of bile duct ligation (BDL). The bile ducts of Sprague-Dawley rats were ligated after 12 hours of fasting and water deprivation. Rat liver samples were collected from three groups of rats at week 1, 2 and 5 after BDL surgery. Three control groups of rats underwent sham operation, including bile duct mobilization, but without BDL. Three biological replicates were used for each group.
2021-09-29 | E-MTAB-10546 | biostudies-arrayexpress
Project description:Background: Vitamin A is an essential nutrient that mammals obtain from dietary carotenoids and retinyl esters. Bile salts aid in the intestinal absorption of vitamin A, after which it is stored in the stellate cells of the liver. Vitamin A-metabolites, such as retinoic acids, are important for cell differentiation, proliferation and immunological processes, and act mostly by activating the nuclear receptors Retinoic Acid Receptor (RAR) and Retinoid Xreceptor (RXR). These receptors also perform key functions in the liver by regulating bile salt, lipid and glucose homeostasisas well is the intrahepatic immune response. Chronic liver diseases are characterized by hepatic vitamin A loss often leading to vitamin A deficiency (VAD). We found that VAD strongly aggravates liver damage in bile duct ligated (BDL) rats and in biliary atresia patients. Here, we performed a transcriptome analysis to characterize the cell biological processes in the rat liver that are disturbed in obstructive cholestasis under VADconditions. Methods: Rats were made VAD by omitting vitamin A from the diet for 16 weeks, followed by ligation of the common bile duct (BDL). 7 days later, the animals were sacrificed. During the 7 days of BDL, half of the animals received daily IP injections with retinyl-palmitate (vitamin A therapy). Bile salt concentrations and liver damage markers (AST/ALT) were determined in serum. Whole genome gene expression in liver tissue was analyzed with the Illumina platform RatRef-12 beadchip. False discovery rate (FDR) was set at a stringent 1%. Data were confirmed by quantitative real time PCR, Western blotting and/or histochemistry. Results: BDL induced dramatic liver damage in VAD rats with serum liver damage markers (AST/ALT)approximately 10-fold increased compared to BDL rats receiving a vitamin A-sufficient (VAS) diet. Only 20 genes were differentially expressed between sham-treated VAS and VAD rats and clustered in the vitamin A metabolism, immune response, carbohydrate and lipid homeostasis. In contrast, 1583 genes were differentially expressed between the BDL-treated VAS and VAD rats. The strongest effects were observed in genes from the vitamin A metabolism, immune response, collagen production and oxidative stress response. Importantly, all the liver damage markers were efficiently reversed by retinyl-palmitate therapy, which was mirrored by an almost complete normalisation of the transcript profile in VAS-BDL rats. Conclusions: We conclude that vitamin A deficiency dramatically aggravates liver damage caused by obstructive cholestasis. The transcriptome analysis suggests that a disturbed immune response may be the predominant causative factor.
2025-01-01 | GSE37313 | GEO
Project description:Liver fibrosis is a common pathological complication of end-stage liver disease, which is usually associated with chronic liver inflammation and injury. Liver fibrosis was induced by bile duct ligation (BDL) in rats. The differentially expressed genes in liver tissue of BDL rats were identified by microarray technique.
2021-05-09 | GSE174099 | GEO
Project description:The farnesoid X receptor (FXR) is a nuclear receptor activated by bile acids and regulates bile acid metabolism, glucose and cholesterol homeostasis. From mouse studies we know that the novel FXR agonist obeticholic acid (OCA) regulates expression of many genes in the liver, but there is currently no data on the effects of OCA on human liver gene expression. This is especially relevant since the novel FXR agonist OCA is currently tested in clinical trials for the treatment of several diseases, such as nonalcoholic steatohepatitis (NASH), nonalcoholic fatty liver disease (NAFLD) and Type 2 Diabetes. In this study we investigate the effect of OCA treatment on gene expression profiles and localization of FXR to the genome in relevant liver samples. ChIP-Seq for FXR in Liver tissue from 2 male mice treated with OCA/INT-747 (10mg/kg/day) and 2 male mice treated with vehicle (1% methyl cellulose).
2016-01-27 | E-GEOD-73624 | biostudies-arrayexpress
Project description:Infants with neonatal cholestasis are prone to neurodevelopmental deficits including neuromotor function. Accumulation of potentially neurotoxic molecules in the bloodstream including ammonia and bile acids and malabsorption of lipids may affect neurodevelopment in these patients. This study examined neuromotor function and bile acid and lipid composition of the brain in a piglet model of obstructive neonatal cholestasis via bile duct ligation (BDL) surgery. Results showed that BDL piglets had compromised balance and increased liver enzyme levels, liver fibrosis and bile duct proliferation compared to SHAM piglets. Plasma and cerebellum bile acid profiles differed between BDL and SHAM piglets with hyocholic acid and conjugated bile acid forms dominating in the BDL group. In the cerebellum there were different lipid profiles, but similar gene expression profiles between the two groups.
2022-06-01 | GSE180600 | GEO
Project description:Background: The increasing prevalence of chronic liver disease has become a significant global health concern. Pyroptosis leads to cell rupture, releasing large amounts of pro-inflammatory cellular contents and promoting the progression of liver fibrosis. Therefore, targeting pyroptosis may serve as a new strategy for the treatment of chronic liver diseases. Methods: We constructed GSDMD-NTki/wt & Alb-creki/wt mice using CRISPR/Cas9 gene editing technology and induced conditional cell death by doxycycline to construct a mouse model of liver fibrosis. We analyzed differentially expressed genes by RNA sequencing and explored their biological functions. Obeticholic acid was used to assess the modeling effects of fibrosis. Results: Doxycycline-treated GSDMD-NTki/wt & Alb-creki/wt mice showed severe liver damage, vacuolation of hepatocytes, increased collagen fibers, accumulation of lipid droplets, and much stronger expression of genes involved in liver fibrosis development in the liver compared with untreated mice. RNA-sequencing showed that upregulated differentially expressed genes in the GSDMD-NTki/wt & Alb-creki/wt doxycycline-treated group were involved in inflammatory responses, cell activation, and metabolic processes. Obeticholic acid was used to assess the modeling effects of fibrosis. Obeticholic acid treatment of GSDMD-NTki/wt & Alb-creki/wt mice reduced ALT and AST levels, and enhanced anti-fibrotic effects were observed. Conclusions: Our results demonstrated that we successfully constructed a mouse model of liver fibrosis, and GSDMD-NT induced fibrosis by mediating lipid metabolism.
2025-01-11 | GSE252989 | GEO
Project description:Decreased bile secretion in rodents by either ligation of the common bile duct or induction of cirrhosis causes changes in the small intestine, including bacterial overgrowth and translocation across the mucosal barrier. Oral administration of bile acids inhibits these effects. The genes regulated by FXR in ileum suggested that it might contribute to the enteroprotective actions of bile acids. To test this hypothesis, mice were administered either GW4064 or vehicle for 2 days and then subjected to bile duct ligation (BDL) or sham operation. After 5 days, during which GW4064 or vehicle treatment was continued, the mice were killed and their intestines were analyzed for FXR target gene expression. Mice were treated with or without FXR ligand GW4064 for 2 days prior to bile duct ligation surgery and for 5 days after surgery. After 5 days the mice were sacrificed and the ileum collected and processed for gene expression analysis. Gene expression in the ilium from each sample group was assayed in duplicate using Affymetrix Mouse Genome 430A 2.0 Gene Chips.
2012-09-12 | E-GEOD-40821 | biostudies-arrayexpress
Project description:Decreased bile secretion in rodents by either ligation of the common bile duct or induction of cirrhosis causes changes in the small intestine, including bacterial overgrowth and translocation across the mucosal barrier. Oral administration of bile acids inhibits these effects. The genes regulated by FXR in ileum suggested that it might contribute to the enteroprotective actions of bile acids. To test this hypothesis, mice were administered either GW4064 or vehicle for 2 days and then subjected to bile duct ligation (BDL) or sham operation. After 5 days, during which GW4064 or vehicle treatment was continued, the mice were killed and their intestines were analyzed for FXR target gene expression.
2012-09-12 | GSE40821 | GEO