Transcriptome sequencing of liver injury models
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ABSTRACT:
PROVIDER: PRJNA1274471 | ENA |
REPOSITORIES: ENA
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Project description:The liver is the largest solid organ and digestive gland in the human body. It plays a key role in the metabolism, transformation and detoxification of the three major organic substances. Therefore, the liver occupies an important place in the body's metabolism of substances. Crizotinib is a new type of drug with high efficiency for the treatment of lung cancer, but it has a large toxic effect, so this paper studies the acute effect of crizotinib on the liver, and studies its key targets for toxic effects through high-throughput transcriptome sequencing, which is divided into normal group and administration group, each group n=3, and the samples are mouse tissue samples.
2025-06-30 | GSE299455 | GEO
Project description:INTRODUCTION Ischemia and reperfusion injury (IRI)-elicited tissue injury contributes to morbidity and mortality in a wide range of pathologies, including myocardial infarction, ischemic stroke, acute kidney injury, trauma, circulatory arrest 1. Ischemia-reperfusion injury is also a major challenge during organ transplantation and cardiothoracic, vascular and general surgery 1. IRI, one of the biggest challenges for organ transplantation, continues to be a vital source of morbidity among recipients, especially in liver transplantation 2. With the enlarging shortage of available donor livers, the increased use of extended criteria donor grafts further increases IRI, adversely affecting both short-term and long-term outcomes of graft and patient survival 3. Numerous studies have investigated the benefits of pharmacological, heat shock, and ischemic preconditioning interventions aimed at decreasing liver IRI 4. However, the benefit was limited. Our center has been making great effort in conquering IRI and have developed a novel surgical technique called ischemia-free liver transplantation 5. It is an ultimate method to overcome IRI in liver transplantation, but there is still a long way to popularize it. As a result, it is still of great significance to study IRI and identify the core genes in the process and the underlying mechanism. Comprehensive bioinformatics analysis has been increasingly important as a method to study various pathological and physiological condition 6. By enrolling multiple omics or combining different types of omics, comprehensive bioinformatics analysis was able to recognize key factors that could have potentially pathogenic impact such as gene expression, protein function, and downstream pathways. With the rapid development of high-throughput sequencing technologies, several transcriptomic datasets on IRI of liver transplantation have become available in the Gene Expression Omnibus (GEO) database. Herein, we recruited 3 GEO datasets to conduct comprehensive analysis with the GEO dataset from our center. Moreover, we performed the first proteome of liver tissues to study liver IRI. Then the transcriptome and proteome were used for combined analysis to reveal key factors in liver IRI.
2022-02-23 | PXD010812 | Pride
Project description:Transcriptional alterations during different stages of hepatic stellate cell activation were determined using RNA Sequencing. Models include acute liver injury (1 injection of CCl4) and chronic liver injury (8 injections of CCl4 over 4-week period) with different recovery timepoints. Illumina NextSeq 500 High was used for sequencing.
2021-12-15 | GSE176042 | GEO
Project description:<p>The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) has established the Drug-Induced Liver Injury Network (DILIN) to collect and analyze cases of severe liver injury caused by prescription drugs, over-the-counter drugs, and alternative medicines, such as herbal products and supplements.</p>
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Project description:Gefitinib induced liver damage+liver Transcriptome sequencing
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Project description:We previously showed that severe liver diseases are characterized by expansion of liver progenitor cells (LPC), which correlates with disease severity. However, the origin and role of LPC in liver physiology and in the hepatic response to injury remains a contentious topic. We have now used genetic lineage tracing of Hnf1β-expressing biliary duct cells to assess their contribution to LPC expansion and hepatocyte generation during normal liver homeostasis, and following different types of liver injury. We found that ductular reaction cells in human cirrhotic livers express HNF1β. However, HNF1β expression was not present in newly generated EpCAM-positive hepatocytes. Using a tamoxifen-inducible Hnf1βCreER/R26RYFP/LacZ mouse, we show that there is no contribution of the biliary epithelium to hepatocyte turnover during liver homeostasis in healthy mice. Moreover, after loss of liver mass, Hnf1β+ LPC did not contribute to hepatocyte regeneration. We also assessed the contribution of Hnf1β+ cells following acute and repeated liver injury. All animal models showed expansion of LPC, as assessed by immunostaining and gene expression profile of sorted YFP-positive cells. A contribution of Hnf1β+ LPC to hepatocyte generation was not detected in animal models of liver injury with preserved hepatocyte regenerative potential such as acute acetaminophen, carbon tetrachloride injury, or chronic diethoxycarbonyl-1,4-dihydro-collidin (DDC)-diet. However, in mice fed with choline-deficient ethionine-supplemented (CDE)-diet, which causes profound hepatocyte damage and arrest, a small number of hepatocytes were derived from Hnf1β+ cells. Conclusion: Hnf1β+ cells do not participate in hepatocyte turnover in the healthy liver or during liver regeneration after partial hepatectomy. After liver injury, LPC arise from the biliary duct epithelium, which gives rise to a limited number of hepatocytes only when hepatocyte regeneration is compromised. Transcriptomic profile using MoGeneST-2.0 chip from 3 samples of YFP+ CDE, 3 samples of YFP+ DDC, 2 samples of YFP+ UTR and 3 samples YFP-
2016-07-03 | E-GEOD-51389 | biostudies-arrayexpress
Project description:Internal organs heal injuries with new connective tissue. However the cellular and molecular events, and the sources of this tissue, remain obscure. Here we tagged extracellular matrix around the mesothelium lining various mouse tissues: peritoneum, liver, and cecum, and applied various injury models. We discovered that preexisting matrix is transferred across organs into wounds. Using proteomics, genetic lineage-tracing and by selectively injuring juxtaposed organs, we demonstrate that the matrix tissue of origin likely dictates the final healing outcome: whether scarring or regeneration.
2022-05-20 | PXD031766 | Pride
Project description:Objective: The present study is aimed to study the liver injury in xylazine poisoning and uncover the underlying mechanism. Method: Forty male SD rats were randomly dived into four groups, control (saline), low dose (10mg/kg xylazine), median dose (20mg/kg xylazine) and high dose (40mg/kg xylazine). And the rats were injected the drug intraperitoneal continuous 28 days, and then collected serum and liver tissues, Elisa, RNA sequencing, histopathology examination, RT-qPCR were performed. Results: Compared to the control group, the body weight of 40mg/kg group was decreased, the level of ALT and AST in serum of 40mg/kg group was increased. Histopathological examination showed fatty degeneration, necrosis and fibrosis of the liver. 192 up-regulated and 277 down-regulated genes were identified through RNA sequencing in the 40mg/kg group and the PPAR signaling pathway ranked first in the KEGG pathway analysis, The common DEG in the 10mg/kg and 40mg/kg (Lox), four common DEGs in the 20mg/kg and 40mg/kg (Srebf1, Nr1dl, Fasn, SCD1), and four genes PCK1, FABP5, ACOX2, CPT2 in the PPAR signaling pathway in the 40mg/kg group were validated through Real-Time PCR Analysis. Conclusion：Long term xylazine injection can cause liver injury and the PAPR signaling pathway play a core role in the process of xylazine related liver injury.
2025-01-02 | GSE271044 | GEO
Project description:Identification of genes and causal mutations regulating growth and fatness traits in pig. Transcriptome sequencing of 10 liver samples of two groups of divergent pigs for growth and fatness.
2016-06-01 | E-GEOD-75850 | biostudies-arrayexpress