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Expression data from patients of idiopathic portal hypertension

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Kohei Kotani

PROVIDER: E-GEOD-69601 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from patients of idiopathic portal hypertension

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

Transcriptomic signatures of progressive and regressive liver fibrosis and portal hypertension

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.

2024-02-13 | E-MTAB-13804 | biostudies-arrayexpress

Portal Hypertension Induced Changes in Splenic Gene Expression

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.

2018-11-21 | GSE113613 | GEO

Portal Hypertension Induced Changes in Splenic microRNA Expression

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

Liver expression data from 1 week old mouse portal tracts

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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GIMAP5 maintains liver sinusoidal endothelial cell identity and prevents portal hypertension

Project description:Chronic liver disease is a major leading cause of portal hypertension that affects approximately 1.5 billion people globally. We show that GIMAP5, a small organellar GTPase, is selectively expressed in liver endothelial cells and human GIMAP5 deficiency causes portal hypertension with capillarization of liver sinusoidal endothelial cells (LSECs). LSEC capillarization is recapitulated in GIMAP5 loss-of-function (LOF) mice, and upon conditional Gimap5 deletion in endothelial cells. Single cell RNA-sequencing analyses reveals replacement of LSECs with capillarized endothelial cells and expansion of liver lymphatic endothelial cells in GIMAP5 LOF mice, and places GIMAP5 upstream of GATA4, a transcription factor required for LSEC-specification. Our studies reveal that GIMAP5 prevents portal hypertension by maintaining LSEC identity and suggest that LSEC is an induced endothelial cell state.

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Liver expression data from 1 week old mouse portal tracts

2014-11-05 | GSE62991 | GEO

Portal Hypertension Induced Changes in Splenic microRNA Expression

Project description:Portal Hypertension Induced Changes in Splenic microRNA Expression

| PRJNA453394 | ENA

Portal Hypertension Induced Changes in Splenic Gene Expression

Project description:Portal Hypertension Induced Changes in Splenic Gene Expression

| PRJNA453393 | ENA

Whole genome profiling of liver biopsies discloses potential biomarkers for diagnosis of idiopathic non-cirrhotic portal hypertension

Project description:Background. Idiopathic non-cirrhotic portal hypertension (INCPH) is a frequently misdiagnosed cause of portal hypertension. It also lacks a specific test for its diagnosis. This study evaluates whether using new immunohistochemistry makers derived from whole genome analysis improves the diagnosis of INCPH. Methods. We analyzed formalin-fixed, paraffin embedded (FFPE) liver tissue from 18 INCPH and 22 patients with cirrhosis (LC) as well as from 14 histologically normal livers (HNL) as controls. Microarray experiments were performed using Illumina Whole-Genome DASL HT BeadChip arrays. Selected genes showing differential expression at Illumina were confirmed using quantitative real-time PCR (qRT-PCR) gene expression performed with Fluidigm Biomark HD system in a subgroup of samples. Immunohistochemistry was used to confirm the qRT-PCR results. Results. At Illumina, a total of 292 genes were differentially expressed (FC>+2/-2 and p-value <0.05) in INCPH compared to the control group (LC and HNL) (202 up-regulated and 90 down-regulated).

2018-03-31 | GSE77627 | GEO

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