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The effect of PLVAP knockdown in human liver sinusoidal endothelial cells (LSECs).

ABSTRACT: To investigate the phenotypic consequences of PLVAP presence/absence in human LSEC, we utilised siRNA knockdown in 3 independent LSEC donors. We then performed gene expression profiling analysis using data obtained from RNA-seq of LSEC with siRNA knockdown of PLVAP and siRNA Negative Control cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE222993 | GEO | 2023/09/15

REPOSITORIES: GEO

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VEGF-A stimulated gene expression in human liver sinusoidal endothelial cells

Project description:Transcriptomic analysis of VEGF-A stimulated liver sinusoidal endothelial cell gene expression. Untreated cells were compared to those treated with VEGF-A. VEGF-A stimulation is critical for normal LSEC phenotype, and the response to liver injury Two conditions: untreated vs. VEGF-A treated. LSEC from 2 donors were pooled. 4 technical repeats.

2013-06-01 | E-GEOD-41110 | biostudies-arrayexpress

Analysis of liver sinusoidal endothelial cells (LSECs) with β-catenin (Ctnnb1) activation

Project description:Endothelial-derived Wnt/Ctnnb1-signaling is an important angiocrine regulator. Ctnnb1 gain-of-function (GOF) in liver sinusoidal endothelial cells was generated by crossing Clec4g-iCre (Wohlfeil SA et al, 2019, Cancer Research) with Ctnnb1(Ex3) fl/fl mice (Harada N et al, 1999, EMBO J) to analyze the effects of endothelial β-catenin signaling on LSEC differentiation and liver function We used microarrays to detail the global programme of gene expression in liver sinusoidal endothelial cells with β-catenin (Ctnnb1) gain-of-function compared to control animals.

2021-11-18 | GSE175777 | GEO

Liver sinusoidal endothelial cells (LSECs) modifications in patients with chronic hepatitis C.

Project description: Not available

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Normal and injured liver sinusoidal endothelial cells

Project description:Comparison of C57BL/6J 8-10 weeks male mouse liver sinusoidal endothelial cells (LSEC) from normal liver and from liver injured by carbon tetrachloride administration. Keywords: other

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Whole genome profiling of liver sinusoidal endothelial cells (LSEC) before and after hepatectomy

Project description:compare acute gene expression changes in LSEC after hepatecomy WT C57BL/6N mice were either sham operated or underwent 2/3 hepatectomy. One day after operation, LSEC were isolated. RNA were immediatedly extracted for gene array.

2013-08-26 | E-GEOD-50046 | biostudies-arrayexpress

Normal and injured liver sinusoidal endothelial cells

2004-10-01 | GSE1689 | GEO

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.

2021-03-01 | GSE158988 | GEO

PROTEOMIC ANALYSIS OF DYSFUNCTIONAL LIVER SINUSOIDAL ENDOTHELIAL CELLS REVEALS SUBSTANTIAL DIFFERENCES IN MOST COMMON EXPERIMENTAL MODELS OF CHRONIC LIVER DISEASES.

Project description:Molecular markers of dedifferentiation of dysfunctional liver sinusoidal endothelial cells (LSEC), have not been fully elucidated. We aimed at deciphering the molecular profile of dysfunctional LSEC in different pathological scenarios. Flow cytometry was used to sort CD11bˉ/CD32b+ and CD11bˉ/CD32bˉLSEC from three rat models of liver disease (bile duct ligation-BDL, inhaled carbon tetrachloride-CCl4 and high fat glucose/fructose diet-HFGFD). Full proteomic profile was performed applying nano-scale liquid chromatography tandem mass spectrometry (nLC-MS) and analyzed with PEAKS software. The percentage of CD32bˉ LSEC varied across groups, suggesting different capillarization processes. Both CD32+ and CD32bˉLSEC from models are different from control LSEC but differently expressed proteins in CD32bˉLSEC are significantly higher. Heatmaps evidenced specific protein expression patterns for each model. Analysis of biological significance comparing dysfunctional CD32bˉLSEC with specialized CD32b+ LSEC from controls showed central similarities represented by 45 common downregulated proteins involved in the suppression of the endocytic machinery and 63 common upregulated proteins associated with the actin-dependent cytoskeleton reorganization. In summary, substantial differences but also similarities in dysfunctional LSEC from the three most common models of liver disease were found, supporting the idea that LSEC may harbor different protein expression profiles according to the etiology or disease stage.

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Expression data of Gata4 endothelial cell-subtype specific knockout primary murine liver sinusoidal endothelial cells

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2020-09-15 | GSE141001 | GEO

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