Liver expression data from 1 week old mouse portal tracts
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE62991 | GEO | 2014/11/05
SECONDARY ACCESSION(S): PRJNA266378
REPOSITORIES: GEO
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Project description:Intrahepatic biliary and arterial development proceed with complex orchestrations involving Notch, TgfB, Wnt and Vegf signaling within the portal tracts of the liver. These pathways coordinate morphogenesis and remodeling temporally and spatially from mid-gestation through early postnatal life. We used microarrays to examine changes in remodeling/differentiation programs in portal tracts at 1 week postanally, comparing Jag1+/-Rfng+/- and controls.
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Project description:Idiopathic portal hypertension (IPH) is characterized by portal hypertension due to obstruction or stenosis of the intrahepatic peripheral portal branches. Researchers have suggested that IPH may be attributed to intrahepatic peripheral portal vein thrombosis, splenic factors, abnormal autoimmunity, and related factors, however, the etiology of IPH remains unclear. We used microarrays to identify the functions of genes expressed in blood samples from patients with IPH.
2015-06-06 | GSE69601 | GEO
Project description:Idiopathic portal hypertension (IPH) is characterized by portal hypertension due to obstruction or stenosis of the intrahepatic peripheral portal branches. Researchers have suggested that IPH may be attributed to intrahepatic peripheral portal vein thrombosis, splenic factors, abnormal autoimmunity, and related factors, however, the etiology of IPH remains unclear. We used microarrays to identify the functions of genes expressed in blood samples from patients with IPH. In order to examine the specific expression of genes in patients with IPH, we analyzed blood samples from three patients with IPH and three healthy volunteers as control using DNA microarrays.
2015-06-06 | E-GEOD-69601 | biostudies-arrayexpress
Project description:Background & Aims: Chronic hepatitis C virus (HCV) infection is complicated by hepatic fibrosis. Hypothesizing that fibrogenic signals may originate in cells susceptible to HCV infection, gene expression of hepatocytes was analyzed from persons with chronic HCV at different stages of liver fibrosis. Methods: HCV-infected subjects with significant liver fibrosis (Ishak fibrosis ≥3) were matched for age, race, and gender to subjects with minimal fibrosis (Ishak fibrosis 0-1). RNA from portal tracts and hepatic parenchyma was isolated from biopsies by laser capture and transcriptome profiling was performed using hybridization arrays. Results: Portal tracts from both groups were enriched for immune related genes when compared to hepatocytes but high fibrosis subjects showed a loss of this enrichment. Hepatocytes from persons with high fibrosis were depleted for genes involved in small molecule and drug metabolism, especially butyrylcholinesterase (BCHE), a gene involved in the metabolism of drugs of abuse. Differential expression of BCHE was validated in the same tissues using qPCR. Cross-sectional and longitudinal testing in an expanded cohort of HCV-infected individuals showed that serum BCHE activity decreased in advance of progression to fibrosis. Conclusion: Chronic HCV infection is associated with a loss of hepatocyte metabolic function, decreased enrichment of immune-related genes in portal tracts and downregulation of BCHE in hepatocytes. Our results indicate that BCHE may be involved in the progression of fibrosis during HCV infection among injection drug users and may serve as a useful marker for fibrosis progression.
2013-08-13 | GSE33650 | GEO
Project description:Background & Aims: Chronic hepatitis C virus (HCV) infection is complicated by hepatic fibrosis. Hypothesizing that fibrogenic signals may originate in cells susceptible to HCV infection, gene expression of hepatocytes was analyzed from persons with chronic HCV at different stages of liver fibrosis. Methods: HCV-infected subjects with significant liver fibrosis (Ishak fibrosis M-bM-^IM-%3) were matched for age, race, and gender to subjects with minimal fibrosis (Ishak fibrosis 0-1). RNA from portal tracts and hepatic parenchyma was isolated from biopsies by laser capture and transcriptome profiling was performed using hybridization arrays. Results: Portal tracts from both groups were enriched for immune related genes when compared to hepatocytes but high fibrosis subjects showed a loss of this enrichment. Hepatocytes from persons with high fibrosis were depleted for genes involved in small molecule and drug metabolism, especially butyrylcholinesterase (BCHE), a gene involved in the metabolism of drugs of abuse. Differential expression of BCHE was validated in the same tissues using qPCR. Cross-sectional and longitudinal testing in an expanded cohort of HCV-infected individuals showed that serum BCHE activity decreased in advance of progression to fibrosis. Conclusion: Chronic HCV infection is associated with a loss of hepatocyte metabolic function, decreased enrichment of immune-related genes in portal tracts and downregulation of BCHE in hepatocytes. Our results indicate that BCHE may be involved in the progression of fibrosis during HCV infection among injection drug users and may serve as a useful marker for fibrosis progression. Liver tissues were chosen from five subjects with chronic HCV infection and Ishak fibrosis stage 3-5 who had sufficient tissue stored in OCT and no HIV infection. Tissues that were stored in TrizolM-BM-. or other lysis buffers were excluded to avoid homogenization of transcriptomes between cellular constituents. Five control tissues were selected from persons of the same race and gender with chronic HCV infection estimated to be of similar duration (by age matching) but whose baseline Ishak fibrosis score was 0-1. One high fibrosis case was later excluded because the subject was found to be HBsAg positive, leaving a total of nine subjects.
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Project description:Splenomegaly is caused by several pathological conditions, including portal hypertension, which is most frequently caused by chronic liver disease (e.g., liver cirrhosis). The detailed mechanisms through which portal pressure induces splenomegaly and the precise pathophysiological conditions in portal hypertension-induced splenomegaly remain to be fully elucidated. We used microarrays to identify the differential gene expression underlying the portal hypertension-induced splenomegaly.
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Project description:Splenomegaly is caused by several pathological conditions, including portal hypertension, which is most frequently caused by chronic liver disease (e.g., liver cirrhosis). The detailed mechanisms through which portal pressure induces splenomegaly and the precise pathophysiological conditions in portal hypertension-induced splenomegaly remain to be fully elucidated. We used microarrays to identify the differential microRNA expression underlying the portal hypertension-induced splenomegaly.
2018-11-21 | GSE113612 | GEO
Project description:Mutations of isocitrate dehydrogenase (IDH) 1 or 2 occur in 10-30% of intrahepatic cholangiocarcinomas (ICCs). However, their functional roles in biliary carcinogenesis are still unknown. We used microarrays to investigate how mutant IDH1 affect the gene expression of intrahepatic biliary organoids generated from normal murine liver.
2019-07-31 | GSE134760 | GEO
Project description:Current model systems for studying intrahepatic biliary disease fail to recapitulate the architecture of intrahepatic bile ducts. Organoids from intrahepatic cholangiocytes can with a new culture method grow with a branching pattern resembling the structure of intrahepatic bile ducts. This dataset contains data from samples of these organoids and from control organoids cultured without this technique. Culture have been performed using isotope labeled amino acids to help distinguish cell derived proteins from the basement membrane extract used as a culture substrate for the organoids.
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Project description:Persistent liver injury triggers a fibrogenic program that causes pathologic remodelling of the hepatic microenvironment (i.e., liver fibrosis) and portal hypertension. The dynamics of gene regulation during liver disease progression and regression remain understudied. Here, we generated hepatic transcriptome profiles in two well-established liver disease models at peak fibrosis and during spontaneous regression after the removal of the inducing agents. We linked the dynamics of key liver disease readouts, such as portal pressure, collagen proportionate area, and transaminase serum levels, to most differentially expressed genes, enabling the identification of transcriptomic signatures of progressive vs. regressive liver fibrosis and portal hypertension. These candidate biomarkers (e.g., Scube1, Tcf4, Src, Hmga1, Trem2, Mafk, Mmp7) were also validated in RNA-seq datasets of patients with cirrhosis and portal hypertension. Finally, deconvolution analysis identified major cell types and suggested an association of macrophage and portal hepatocyte signatures with portal hypertension and fibrosis area in both models.
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