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

ABSTRACT: compare acute gene expression changes in LSEC after hepatecomy

ORGANISM(S): Mus musculus

PROVIDER: GSE50046 | GEO | 2013/08/26

SECONDARY ACCESSION(S): PRJNA215862

REPOSITORIES: GEO

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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

Gene expression profiles in fetal human liver sinusoidal endothelial cells (LSEC)

Project description:Understanding molecular fingerprints of specific cell types is central for defining lineage development, progression, differentiation and pathophysiological perturbations. This study addressed gene expression profiles in freshly isolated fetal human LSEC as well as these LSEC after cell culture. Comparisons with human umbilical vein endothelial cells (HUVEC) allowed determination of lineage-specific differences. Cell culture allowed identification of differences in phenotype regulation of cells under these conditions.

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Normal and injured liver sinusoidal endothelial cells

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

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Normal and injured liver sinusoidal endothelial cells

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

Project description: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.

2023-09-15 | GSE222993 | 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.

2023-10-24 | PXD040661 | Pride

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 sinusoidal endothelium: a microenvironment-dependent differentiation program in rat including the novel junctional protein liver endothelial differentiation-associated protein-1

Project description:Liver sinusoidal endothelium (LSEC) is a prime example for organ-specific microvascular differentiation and functions. Disease-associated capillarization of LSEC in vivo and dedifferentiation of LSEC in vitro indicate the importance of the hepatic microenvironment. To identify the LSEC-specific molecular differentiation program in the rat, we used a two-sided gene expression profiling approach comparing LSEC freshly isolated ex vivo with both lung microvascular endothelial cells (LMEC) and with LSEC cultured for 42h. The LSEC signature consisted of 48 genes both down-regulated in LMEC and in LSEC upon culture (FC>7 in at least one comparison); qRT-PCR confirmation of these genes included numerous family members and signalling pathway-associated molecules. The LSEC differentiation program comprised distinct sets of growth (wnt2, Fzd4, 5, 9, wls, VEGFR1, 2, 3, Nrp2) and transcription factors (Gata4, Lmo3, Tcfec, Maf) as well as endocytosis-related (Stabilin-1/2, Lyve1 and Ehd3) and cytoskeleton-associated molecules (Rnd3/RhoE). Specific gene induction in cultured LSEC versus freshly isolated LSEC as well as LMEC (Esm-1, Aatf) and up-regulation of gene expression to LMEC levels (CXCR4, Apelin) confirmed true transdifferentiation of LSEC in vitro. In addition, our analysis identified a novel 26 kDa single-pass transmembrane protein, liver endothelial differentiation-associated protein (Leda)-1, that was selectively expressed in all liver endothelial cells and preferentially localized to the abluminal cell surface. Upon forced over-expression in MDCK cells, Leda-1 was sorted baso-laterally to E-cadherin-positive adherens junctions suggesting functional involvement in cell adhesion and polarity. Conclusion: Comparative microvascular analysis in rat identified a hepatic microenvironment-dependent LSEC-specific differentiation program including the novel junctional molecule Leda-1.

2010-03-15 | GSE20375 | GEO

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