E-GEOD-39157
Ontology highlight
ABSTRACT:
PROVIDER: E-GEOD-39157 | ExpressionAtlas | 2015-07-08
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:Genome-wide analysis of mRNA expression alterations in human primary hepatocytes compared with cAMP treated and non-treated human embryonic stem cell (hESC) derived hepatic populations
| PRJNA170116 | ENA
Project description:Microarrays were used to examine gene expression differences between primary human hepatocytes and hESC derived hepatoblast cultures treated or non-treated with cAMP. hESC's were differentiated with a hepatic cell lineage specific protocol that included the use of a 3-dimensional cell aggregation culturing technique. Followed by cAMP signaling, this promoted the maturation of hepatoblasts into a more hepatocyte-like population. Importantly, key enzymes related to liver function show that cAMP induced populations have a gene expression profile that is similar to primary human hepatocytes. Total RNA obtained from cultured primary hepatocytes and hESC derived hepatic populations.
2013-07-04 | E-GEOD-39157 | biostudies-arrayexpress
Project description:Microarrays were used to examine gene expression differences between primary human hepatocytes and hESC derived hepatoblast cultures treated or non-treated with cAMP. hESC's were differentiated with a hepatic cell lineage specific protocol that included the use of a 3-dimensional cell aggregation culturing technique. Followed by cAMP signaling, this promoted the maturation of hepatoblasts into a more hepatocyte-like population. Importantly, key enzymes related to liver function show that cAMP induced populations have a gene expression profile that is similar to primary human hepatocytes.
2013-07-04 | GSE39157 | GEO
Project description:We report the genome-wide profiling of FXR binding by ChIP-seq from GW4064 or DMSO treated primary human hepatocytes. We reported altered RNA expression profiles in primary human hepatocypes upon GW4064 treatment compared to DMSO control by RNA-seq. We also reported the altered RNA expression profiles in livers from WT C57BL/6J mice upon GW4064 treatment compared to vehicle control.
2014-07-24 | GSE57227 | GEO
Project description:Genome-wide expression profiling has been performed in malignant HepG2 cells and compared to the expression in normal human hepatocytes. 56 ucRNAs, representing 11% of all ucRNAs analyzed, were aberrantly and significantly (p<0.05) expressed in malignant HepG2 cells compared to non-malignant human hepatocytes.
2010-08-24 | GSE17779 | GEO
Project description:Each cell type responds uniquely to stress and fractionally contributes to global and tissue-specific stress responses. Hepatocytes, liver macrophages (M?), and sinusoidal endothelial cells (SEC) play functionally important and interdependent roles in adaptive processes such as wound healing, obesity, and tumor growth. Although these cell types demonstrate significant phenotypic and functional heterogeneity, their distinctions enabling disease-specific responses remain understudied. To address this, we developed a strategy for simultaneous isolation and quantification of these liver cell types based on antigenic cell surface marker expression in response to DEN and found that while there was only a marginal increase in hepatocyte number, M? and SEC populations were quantitatively increased. Global gene expression profiling of hepatocytes, M? and SEC identified characteristic gene “fingerprints” that define each cell type and their distinct physiological or oncogenic stress signatures. Integration of these cell-specific gene fingerprints with available hepatocellular carcinoma (HCC) patient microarray data demonstrates that the hepatocyte-specific response strongly correlates with the human HCC gene expression profile. Liver-specific M? and SEC gene signatures demonstrate significant alterations in inflammatory and angiogenic gene regulatory pathways, which may impact the hepatocyte response to oncogenic stress. Further validation confirms alterations in components of two key pathways, AP-1 and p53, that have been previously associated with HCC onset and progression. Our data reveal unique gene expression patterns that serve as molecular “fingerprints” for the cell-centric responses to pathologic stimuli in the distinct microenvironment of the liver. The technical advance highlighted in this study provides an essential resource for assessing hepatic cell-specific contributions to oncogenic stress, information that could unveil previously unappreciated molecular mechanisms for the cellular crosstalk that underlies the development of hepatic cancer. Total RNA isolated from each specific cell type (Hepatocyte (PH), Sinusoidal Endothelial Cell (SEC), and Macrophage (MP)) pooled from 3-4 DEN-treated mice and compared to their untreated counterparts.
2015-09-20 | E-GEOD-67225 | biostudies-arrayexpress
Project description:Aim of the study was to characterize at a molecular level (changes in transcriptomes) the crosstalk between tumor hepatocytes and activated hepatic stellate cells (HSC) in liver cancer. This was adressed by using a coculture model system of HepaRG cell line (tumor hepatocytes, human), and LX2 cell line (HSC, human). By using genome-wide expression profiling, we demonstrated that hepatocyte-HSC crosstalk is bidirectional and results in the deregulation of functionally relevant gene networks.
2012-06-01 | GSE32565 | GEO
Project description:The ever-increasing therapeutic and pharmaceutical demand for liver cells calls for systems that enable mass production of hepatic cells. Here we describe a large-scale suspension system that uses human endoderm stem cells (hEnSCs) as precursors to generate functional and transplantable hepatocytes (E-heps) or cholangiocytes (E-chos). hEnSC-derived hepatic populations are characterized by single-cell transcriptomic analyses and compared with hESC-derived counterparts, in-vitro-maintained or -expanded primary hepatocytes and adult cells, which reveals that hepatic differentiation of hEnSCs recapitulates in vivo development and that the heterogeneities of the resultant populations can be manipulated by regulating the EGF and MAPK signaling pathways. Functional assessments demonstrate that E-heps and E-chos possess properties comparable with adult counterparts and that, when transplanted intraperitoneally, encapsulated E-heps were able to rescue rats with acute liver failure. Our study lays the foundation for cell-based therapeutic agents and in vitro applications for liver diseases.
2021-04-20 | GSE128060 | GEO
Project description:We report the genome-wide profiling of FXR binding by ChIP-seq from GW4064 or DMSO treated primary human hepatocytes. We reported altered RNA expression profiles in primary human hepatocypes upon GW4064 treatment compared to DMSO control by RNA-seq. We also reported the altered RNA expression profiles in livers from WT C57BL/6J mice upon GW4064 treatment compared to vehicle control. Primary human hepatocytes were treated with 5uM GW4064 or DMSO control, 1 hour later, cells were fixed and collected for chromatin isolation. 24 hours post treatment, cells were isolated for RNA isolation. This submission represents HTS component of study.
2014-07-24 | E-GEOD-57227 | biostudies-arrayexpress
Project description:Rifampin causes drug interactions by altering hepatic drug metabolism. Because microRNAs (miRNAs) have been shown to regulate genes involved in drug metabolism, we determined the effect of rifampin on the expression of hepatic miRNAs. Primary human hepatocytes from seven subjects were treated with rifampin, and the expression of miRNA and cytochrome P450 (P450) mRNAs was measured by TaqMan assays and RNA-seq, respectively. Rifampin induced the expression of 10 clinically important and 13 additional P450 genes and repressed the expression of 9 other P450 genes (P < 0.05). Rifampin induced the expression of 33 miRNAs and repressed the expression of 35 miRNAs (P < 0.05). Several of these changes were highly negatively correlated with the rifampin-induced changes in the expression of their predicted target P450 mRNAs, supporting the possibility of miRNA-induced regulation of P450 mRNA expression. In addition, several other miRNA changes were positively correlated with the changes in P450 mRNA expression, suggesting similar regulatory mechanisms. Despite the interindividual variability in the rifampin effects on miRNA expression, principal components analysis clearly separated the rifampin-treated samples from the controls. In conclusion, rifampin treatment alters miRNA expression patterns in human hepatocytes, and some of the changes were correlated with the rifampin-induced changes in expression of the P450 mRNAs they are predicted to target. Primary human hepatocytes were treated rifampin or vehicle for 24 hours. Rifampin-treated samples are not available for the 30Jul10 patient or the Hep2 patient due to raw data file corruption.
2016-04-06 | E-GEOD-79933 | biostudies-arrayexpress