Dataset Information

E-GEOD-39157

ABSTRACT: 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

PROVIDER: E-GEOD-39157 | ExpressionAtlas | 2015-07-08

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-39157-analysis-methods.tsv	Tabular
	E-GEOD-39157-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-39157-configuration.xml	Xml
	E-GEOD-39157-percentile-ranks.tsv	Tabular
	E-GEOD-39157.condensed-sdrf.tsv	Tabular

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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.

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E-GEOD-39157

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