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Gene expression data from bioprinted liver tissues treated with 0.1% DMSO (dimethyl sulfoxide: vehicle), 10 ng/mL transforming growth factor beta 1 (TGF-β1) or 0.209 µM methotrexate (MTX) for either 14 or 28 days.

ABSTRACT: Gene expression data from bioprinted liver tissues comprising primary human hepatocytes (HCs), hepatic stellate cells (HSCs), and human umbilical vein endothelial cells (HUVECs) with and without Kupffer cells (KCs) treated with 0.1% DMSO (dimethyl sulfoxide: vehicle), 10 ng/mL transforming growth factor beta 1 (TGF-β1) or 0.209 µM methotrexate (MTX) for either 14 or 28 days. Agents known to cause fibrotic injury were modeled over an extended period of time in this model system in the standard (-KCs) and modified (+KCs) tissue model to elucidate the role of Kupffer cells in modulating the injury/fibrogenic response over time. Samples are from studies corresponding to 4 independent tissue prints 1-4r

ORGANISM(S): Homo sapiens

PROVIDER: GSE113630 | GEO | 2019/02/13

REPOSITORIES: GEO

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Project description:There is an evident, unmet need to develop a commercially available in vitro system that can model inflammatory states of the liver and predict immune-mediated hepatotoxicity of drugs and xenobiotics taken under inflamed conditions. Hepatocyte-Kupffer cell co-cultures can model inflammation-mediated hepatotoxicity; however, Kupffer cell (KC) source remains an important bottleneck for the development of such models. Primary human Kupffer cells (PHKCs) are costly, limited in availability and exhibit donor variability. An alternative cell source for KCs has not been reported. Important paradigm shift from the classical dogma of adult blood-circulating monocyte-derived macrophages to intrahepatic precursor/fetal monocyte-derived macrophages has shed new light into the origin of KCs in vivo. Based on these recent findings, we report here, a novel method to generate human KCs in vitro from stem cells (hPSC-KCs) via fetal monocytes. hPSC-KCs expressed macrophage markers, CD11, CD14, CD68, CD163 and CD32 at gene and protein level and exhibited functional properties such as phagocytosis and Interleukin-6 and Tumor Necrosis Factor-4alpha production upon activation. Importantly, molecular signature, liver-macrophage specific CLEC-4F expression and cytokines production levels of hPSC-KCs were similar to PHKCs but different from non-liver macrophages. We used an inflammatory liver co-culture model to demonstrate that activated hPSC-KCs, but not non-liver macrophages, were able to recapitulate effects of PHKCs when stimulated with paradigm hepatotoxicants. hPSC-KCs developed in this study offer a renewable human cell source for liver-specific macrophages which can be used to develop in vitro systems for modelling the inflammatory state of the liver. Gene expression profiles of 9 samples were determined using Human Gene 2.0 ST Array. These 9 samples included three replicates each of PHKCs (primary human Kupffer cells), human pluripotent stem cell-dervied Kupffer cells (hPSC-KCs) and non-liver macrophages (NL-Mφ).

Dataset Information

Gene expression data from bioprinted liver tissues treated with 0.1% DMSO (dimethyl sulfoxide: vehicle), 10 ng/mL transforming growth factor beta 1 (TGF-β1) or 0.209 µM methotrexate (MTX) for either 14 or 28 days.

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