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Portal Hypertension Induced Changes in Splenic Gene Expression

ABSTRACT: 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.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE113613 | GEO | 2018/11/21

REPOSITORIES: GEO

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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.

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Transcriptomic signatures of progressive and regressive liver fibrosis and portal hypertension

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

Infusion of human amniotic epithelial and mesenchymal stromal stem cells as a new therapeutic option for portal hypertension and cirrhosis

Project description:Background and aims. Portal hypertension is the main consequence of cirrhosis, responsible for the complications defining clinical decompensation. The only cure for decompensated cirrhosis is liver transplantation, but it is a limited resource and opens the possibility of regenerative therapy. We investigated the potential of human amniotic membrane-derived mesenchymal stromal (hAMSCs) and epithelial (hAECs) stem cells for the treatment of portal hypertension and chronic liver disease. Methods. In vivo: hAMSCs and hAECs were isolated from human amniotic membranes. Cirrhotic rats with ascites (chronic CCl4 inhalation) received 4x10e6 hAMSCs, 4x10e6 hAECs, or vehicle (NaCl 0.9%) (intraperitoneal; n=10 per group). After 2-week we analyzed: a) portal pressure (PP) and liver microcirculatory function; b) liver sinusoidal endothelial (LSECs) and hepatic stellate (HSCs) cells phenotype; c) hepatic fibrosis, inflammation and hepatic function. In vitro: HSCs isolated from CCl4-cirrhotic rats were co-cultured with hAMSCs, hAECs or vehicle for 24h. RNA profile was analyzed by RNAseq. Results. Cirrhotic rats receiving hAMSCs or hAECs had significantly lower PP than vehicle-treated animals, together with improved liver microcirculatory function. This hemodynamic amelioration was associated with improvement in LSECs capillarization and HSCs de-activation, although hepatic collagen/fibrosis was not significantly reduced. Rats that received placenta derived stem cells had markedly reduced hepatic inflammation and oxidative stress. Finally, liver function tests significantly improved in rats receiving hAMSCs. In vitro experiments confirmed HSCs de-activation when co-cultured with stem cells. Conclusion. This pre-clinical study shows that infusion of human amniotic stem cells effectively decreases PP by ameliorating liver microcirculation, suggesting that it may represent a new treatment option for advanced cirrhosis with portal hypertension.

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GIMAP5 maintains liver sinusoidal endothelial cell identity and prevents portal hypertension

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Expression data from patients of idiopathic portal hypertension

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Portal Hypertension Induced Changes in Splenic Gene Expression

Project description:Portal Hypertension Induced Changes in Splenic Gene Expression

| PRJNA453393 | ENA

Portal Hypertension Induced Changes in Splenic microRNA Expression

Project description:Portal Hypertension Induced Changes in Splenic microRNA Expression

| PRJNA453394 | 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).

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Proteomic profile in the diagnostics of portal hypertension in patients with compensated advanced liver disease

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2024-02-01 | PXD040807 | Pride

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